The study suggests that milk is one of the best sources of vitamin B12
The Daily Telegraph has reported that “two glasses of milk a day could help protect against Alzheimer's”. The newspaper says that research has shown that “milk is one of the best sources of vitamin B12, which is thought to reduce neurological damage to the brain”. The study is also reported to have found that elderly patients with low levels of vitamin B12 had twice the amount of brain shrinkage found in people with higher levels of the vitamin.
The findings described in the newspaper come from two different studies by the same research group. The findings on B12 levels and brain shrinkage were reported in 2008, while the current study examines how dietary sources of vitamin B12 relate to B12 levels found in the body. While the research suggests that milk and fish are good sources of B12, the study has some limitations and will need to be confirmed by further research.
This study did not look at the effects of milk consumption on brain shrinkage or Alzheimer’s disease, and further research would be needed to determine whether drinking milk can ease these conditions. However, maintaining adequate levels of vitamins through a balanced diet is important for overall health.
Where did the story come from?
Dr Anna Vogiatzoglou and colleagues from the University of Oxford and universities in Norway carried out this research, which was published in the peer-reviewed American Journal of Clinical Nutrition.
The study was funded by a number of Norwegian organisations, including the Norwegian Health Association, the Foundation to Promote Research into Functional Vitamin B12 deficiency, the Research Council of Norway plus the Alzheimer’s Research Trust and the Charles Wolfson Charitable Trust in the UK.
See complete:
http://www.nhs.uk/news/2009/03March/Pages/MilkAlzheimers.aspx
Tuesday, March 17, 2009
Friday, March 6, 2009
Sunday, February 22, 2009
Aging facts
In January 2006, the first of 78 million “baby boomers” began to turn 60. Currently there are 34.9 million Americans aged 65 and older, comprising 12.4% of our population. The number of those 65 or older will double to 70.3 million by 2030. The 85+ population is projected to increase from 4.6 million in 2002 to 9.6 million in 2030.
Persons reaching age 65 have an average life expectancy of an additional 18.1 years (19.4 years for females, 16 years for males).
Within a decade, an aging America will spend one of every five dollars on health care. The nation’s total health care bill is expected to tally more than $4 trillion by 2015, accounting for one fifth of gross domestic product. In 2004, $1.87 trillion was spent on health care. Public and private health care spending is expected to reach about $12,320 per capita in 2015, compared with $6,683 in 2005. Medicare spending will reach $792 billion in 2015, compared with $309 billion in 2004.
Age-Related Diseases
Even though people are living longer than ever, diseases of aging continue to affect many older men and women, seriously compromising the quality of their lives and their economic well being.
Government statistics show that more than half of all Americans over age 65 show evidence of osteoarthritis in at least one joint. More than half of Americans over age 50 have osteoporosis or low bone mass. Cancer, in nearly all of its forms, is directly linked to aging; 77% of all malignancies are diagnosed after the age of 55. An estimated 4.5 million Americans have Alzheimer's disease; one in 10 individuals over 65 and nearly half of those over 85 are affected. It costs taxpayers three times as much to treat an Alzheimer's patient as any other Medicare patient. One out of every 100 persons over the age of 60 suffers from Parkinson’s disease with 600,000 new cases being diagnosed each year. Each year about 700,000 people experience a new or recurrent stroke. Stroke is the leading cause of serious, long-term disability in the United States.
http://www.buckinstitute.org/site/index.php?option=com_content&task=view&id=15&Itemid=136
Persons reaching age 65 have an average life expectancy of an additional 18.1 years (19.4 years for females, 16 years for males).
Within a decade, an aging America will spend one of every five dollars on health care. The nation’s total health care bill is expected to tally more than $4 trillion by 2015, accounting for one fifth of gross domestic product. In 2004, $1.87 trillion was spent on health care. Public and private health care spending is expected to reach about $12,320 per capita in 2015, compared with $6,683 in 2005. Medicare spending will reach $792 billion in 2015, compared with $309 billion in 2004.
Age-Related Diseases
Even though people are living longer than ever, diseases of aging continue to affect many older men and women, seriously compromising the quality of their lives and their economic well being.
Government statistics show that more than half of all Americans over age 65 show evidence of osteoarthritis in at least one joint. More than half of Americans over age 50 have osteoporosis or low bone mass. Cancer, in nearly all of its forms, is directly linked to aging; 77% of all malignancies are diagnosed after the age of 55. An estimated 4.5 million Americans have Alzheimer's disease; one in 10 individuals over 65 and nearly half of those over 85 are affected. It costs taxpayers three times as much to treat an Alzheimer's patient as any other Medicare patient. One out of every 100 persons over the age of 60 suffers from Parkinson’s disease with 600,000 new cases being diagnosed each year. Each year about 700,000 people experience a new or recurrent stroke. Stroke is the leading cause of serious, long-term disability in the United States.
http://www.buckinstitute.org/site/index.php?option=com_content&task=view&id=15&Itemid=136
UC SCIENTISTS PROPOSE NEW MODEL FOR ALZHEIMER’S DISEASE
A study from the Buck Institute for Age Research offers a revolutionary new model for Alzheimer’s disease (AD), a devastating neurodegenerative disorder which afflicts 24 million people worldwide. In an effort to unravel the normal function of a protein implicated in AD, scientists in California and France have discovered a naturally occurring protein that provides a new therapeutic target for the disease. The finding upsets the current theory that AD is a disease of toxicity stemming from damage caused by sticky plaques that collect in the brain – this research points to the condition as a disorder involving an imbalance in signaling between neurons. The study appears online in the Nature publication Cell Death and Differentiation.
One of the mysteries of AD has been the normal function of the amyloid precursor protein (APP) which are concentrated at the points where neurons connect. Even though the sticky amyloid plaques which have been viewed as a hallmark sign of AD result from APP, it seems unlikely that APP exists simply to cause Alzheimer’s disease. In their study, scientists from the Buck Institute and the CNRS (Centre Nationale de la Recherche Scientifique) show that APP binds to netrin-1, a protein that helps to guide nerves and their connections in the brain, as well as helping nerve cells to survive. When netrin-1 was given to mice that have a gene for Alzheimer’s disease their symptoms were reversed, and the sticky amyloid was reduced. These results suggest that the long-held belief that AD is caused by brain cell damage inflicted by the amyloid plaques may be wrong; instead, it is beginning to appear that the disease stems from an imbalance between the normal making and breaking of connections in the brain, with netrin-1 supporting the connections and the amyloid breaking the connections -- both by binding to APP and activating normal cell programs. Not only did the netrin-1 binding to APP keep the nerve cells alive and connected, but it also shut down the production of the amyloid, all of which makes it an interesting potential therapeutic.
“I think we’re going to see an explosion in the next five years involving the dissection of these signaling pathways whose imbalance leads to Alzheimer’s disease,” said Buck Institute Faculty Member Dale Bredesen, MD, who led the California half of the French-Californian collaborative research. “We now believe that APP is part of a ‘plasticity module’ that functions in normal memory and forgetting, and that netrin-1 gives us an important starting point to restore the normal balance.”
“We believe that Alzheimer’s disease is somewhat analogous to cancer, which results from an imbalance between the normal processes that support cell survival and those that cause cell turnover,” said Patrick Mehlen, PhD, Director of the Apoptosis, Cancer and Development CNRS Laboratory at the University of Lyon and co-senior author of the study. “Our hope is that this research will lead to therapeutics that will be used to address this imbalance much earlier in the disease process.”
Research is underway to develop a drug based on the findings. The Buck Institute and the CNRS in Lyon are partnering with Neurobiological Technologies Inc., (NASDAQ: NTII) to bring the discovery from the laboratory to clinical trials.
Other researchers involved in the study include first author Filipe Calheiros Lourenço, of the University of Lyon, along with co-workers Joanna Fombonne, Véronique Corset and Fabien Llambi; Verónica Galvan of the Buck Institute, and Ulrike Müller of the University of Heidelberg. The work was supported by the Agence Nationale de la Recherche, the CNRS (Centre Nationale de la Recherche Scientifique), the National Institutes of Health, the Joseph Drown Foundation, the John Douglas French Foundation, and the Alzheimer’s Association.
About the Buck Institute:
The Buck Institute is the only freestanding institute in the United States that is devoted solely to basic research on aging and age-associated disease. The Institute is an independent nonprofit organization dedicated to extending the healthspan, the healthy years of each individual’s life. The National Institute on Aging designated the Buck a “Nathan Shock Center of Excellence in the Biology of Aging,” one of just five centers in the country. Buck Institute scientists work in an innovative, interdisciplinary setting to understand the mechanisms of aging and to discover new ways of detecting, preventing and treating conditions such as Alzheimer’s and Parkinson’s disease, cancer, diabetes and stroke. Collaborative research at the Institute is supported by new developments in genomics, proteomics and bioinformatics technology.
http://www.buckinstitute.org/site/index.php?option=com_content&task=view&id=479
One of the mysteries of AD has been the normal function of the amyloid precursor protein (APP) which are concentrated at the points where neurons connect. Even though the sticky amyloid plaques which have been viewed as a hallmark sign of AD result from APP, it seems unlikely that APP exists simply to cause Alzheimer’s disease. In their study, scientists from the Buck Institute and the CNRS (Centre Nationale de la Recherche Scientifique) show that APP binds to netrin-1, a protein that helps to guide nerves and their connections in the brain, as well as helping nerve cells to survive. When netrin-1 was given to mice that have a gene for Alzheimer’s disease their symptoms were reversed, and the sticky amyloid was reduced. These results suggest that the long-held belief that AD is caused by brain cell damage inflicted by the amyloid plaques may be wrong; instead, it is beginning to appear that the disease stems from an imbalance between the normal making and breaking of connections in the brain, with netrin-1 supporting the connections and the amyloid breaking the connections -- both by binding to APP and activating normal cell programs. Not only did the netrin-1 binding to APP keep the nerve cells alive and connected, but it also shut down the production of the amyloid, all of which makes it an interesting potential therapeutic.
“I think we’re going to see an explosion in the next five years involving the dissection of these signaling pathways whose imbalance leads to Alzheimer’s disease,” said Buck Institute Faculty Member Dale Bredesen, MD, who led the California half of the French-Californian collaborative research. “We now believe that APP is part of a ‘plasticity module’ that functions in normal memory and forgetting, and that netrin-1 gives us an important starting point to restore the normal balance.”
“We believe that Alzheimer’s disease is somewhat analogous to cancer, which results from an imbalance between the normal processes that support cell survival and those that cause cell turnover,” said Patrick Mehlen, PhD, Director of the Apoptosis, Cancer and Development CNRS Laboratory at the University of Lyon and co-senior author of the study. “Our hope is that this research will lead to therapeutics that will be used to address this imbalance much earlier in the disease process.”
Research is underway to develop a drug based on the findings. The Buck Institute and the CNRS in Lyon are partnering with Neurobiological Technologies Inc., (NASDAQ: NTII) to bring the discovery from the laboratory to clinical trials.
Other researchers involved in the study include first author Filipe Calheiros Lourenço, of the University of Lyon, along with co-workers Joanna Fombonne, Véronique Corset and Fabien Llambi; Verónica Galvan of the Buck Institute, and Ulrike Müller of the University of Heidelberg. The work was supported by the Agence Nationale de la Recherche, the CNRS (Centre Nationale de la Recherche Scientifique), the National Institutes of Health, the Joseph Drown Foundation, the John Douglas French Foundation, and the Alzheimer’s Association.
About the Buck Institute:
The Buck Institute is the only freestanding institute in the United States that is devoted solely to basic research on aging and age-associated disease. The Institute is an independent nonprofit organization dedicated to extending the healthspan, the healthy years of each individual’s life. The National Institute on Aging designated the Buck a “Nathan Shock Center of Excellence in the Biology of Aging,” one of just five centers in the country. Buck Institute scientists work in an innovative, interdisciplinary setting to understand the mechanisms of aging and to discover new ways of detecting, preventing and treating conditions such as Alzheimer’s and Parkinson’s disease, cancer, diabetes and stroke. Collaborative research at the Institute is supported by new developments in genomics, proteomics and bioinformatics technology.
http://www.buckinstitute.org/site/index.php?option=com_content&task=view&id=479
What are water-soluble vitamins?
What are water-soluble vitamins?
Water-soluble vitamins include B-complex vitamins and vitamin C. They dissolve in water and are not stored by the body. Excess amounts are eliminated in urine so must be replaced every day in our diet to provide a continuous supply.
Water-soluble vitamins are easily destroyed or washed away during food storage and preparation, but following correct procedures in these two areas can minimise this loss. It's best to refrigerate fresh produce, keep milk and grains away from strong light, and use the cooking water from vegetables to prepare gravy or soups.
Generally, water-soluble vitamins are not harmful as the body excretes excess levels in urine.
B-complex vitamins
B-complex vitamins help the body get energy from food, and are involved in functions such as appetite control, vision, healthy skin, a healthy nervous system and red blood cell formation.
B-complex vitamins:
* B1 - Thiamin
* B2 - Riboflavin
* B3 - Niacin
* B5 - Pantothenic acid
* B6 - Pyridoxine
* B12 - Cobalamin
* Biotin
* Folate (folic acid)
Sources
B-complex vitamins are found in a variety of foods:
* Cereal grains
* Meat
* Poultry
* Fish
* Eggs
* Milk
* Beans and peas
* Fresh vegetables
Vitamin B deficiencies
Visit the Nutrition Foundation for its recommended daily intake of B-complex vitamins. Insufficient levels of vitamin B can cause the following conditions:
Beriberi - due to a lack of thiamin (B1). Symptoms include weight loss, emotional disturbances and weakness or pain in the limbs.
Pellagra - due to a lack of niacin (B3). It can affect the skin, mucous membranes, central nervous system and gastrointestinal system.
Pernicious anaemia - due to a lack of cobalamin (B12). Symptoms include tiredness, palpitations, shortness of breath and dizziness. It can be masked by high doses of folic acid in the diet, which treat the anaemia without treating the B12 deficiency. This can be dangerous because a lack of B12 can eventually lead to neurological damage. B12 deficiency may be a problem in older people when B12 absorption is reduced. Vegans can be at a higher risk of deficiency because of the absence of B12 in plant foods.
If treated at an early stage these deficiencies can be corrected, with most people making a full recovery.
Supplements
Water-soluble vitamins are available as dietary supplements, but a healthy diet will provide sufficient levels of these vitamins. At certain times, such as preconception and early pregnancy, specific folic acid supplements will be required.
High levels of some B vitamins may be harmful, but this is only likely if you take high-dose supplements, and not from natural food sources. For example, high doses of vitamin B6 can cause peripheral neuropathy, resulting in an unstable gait and numbness.
As with all supplements, no more than the dose stated on the package should be taken.
http://www.bbc.co.uk/health/healthy_living/nutrition/dietary_vitwater1.shtml#vitamin_b_deficiencies
Water-soluble vitamins include B-complex vitamins and vitamin C. They dissolve in water and are not stored by the body. Excess amounts are eliminated in urine so must be replaced every day in our diet to provide a continuous supply.
Water-soluble vitamins are easily destroyed or washed away during food storage and preparation, but following correct procedures in these two areas can minimise this loss. It's best to refrigerate fresh produce, keep milk and grains away from strong light, and use the cooking water from vegetables to prepare gravy or soups.
Generally, water-soluble vitamins are not harmful as the body excretes excess levels in urine.
B-complex vitamins
B-complex vitamins help the body get energy from food, and are involved in functions such as appetite control, vision, healthy skin, a healthy nervous system and red blood cell formation.
B-complex vitamins:
* B1 - Thiamin
* B2 - Riboflavin
* B3 - Niacin
* B5 - Pantothenic acid
* B6 - Pyridoxine
* B12 - Cobalamin
* Biotin
* Folate (folic acid)
Sources
B-complex vitamins are found in a variety of foods:
* Cereal grains
* Meat
* Poultry
* Fish
* Eggs
* Milk
* Beans and peas
* Fresh vegetables
Vitamin B deficiencies
Visit the Nutrition Foundation for its recommended daily intake of B-complex vitamins. Insufficient levels of vitamin B can cause the following conditions:
Beriberi - due to a lack of thiamin (B1). Symptoms include weight loss, emotional disturbances and weakness or pain in the limbs.
Pellagra - due to a lack of niacin (B3). It can affect the skin, mucous membranes, central nervous system and gastrointestinal system.
Pernicious anaemia - due to a lack of cobalamin (B12). Symptoms include tiredness, palpitations, shortness of breath and dizziness. It can be masked by high doses of folic acid in the diet, which treat the anaemia without treating the B12 deficiency. This can be dangerous because a lack of B12 can eventually lead to neurological damage. B12 deficiency may be a problem in older people when B12 absorption is reduced. Vegans can be at a higher risk of deficiency because of the absence of B12 in plant foods.
If treated at an early stage these deficiencies can be corrected, with most people making a full recovery.
Supplements
Water-soluble vitamins are available as dietary supplements, but a healthy diet will provide sufficient levels of these vitamins. At certain times, such as preconception and early pregnancy, specific folic acid supplements will be required.
High levels of some B vitamins may be harmful, but this is only likely if you take high-dose supplements, and not from natural food sources. For example, high doses of vitamin B6 can cause peripheral neuropathy, resulting in an unstable gait and numbness.
As with all supplements, no more than the dose stated on the package should be taken.
http://www.bbc.co.uk/health/healthy_living/nutrition/dietary_vitwater1.shtml#vitamin_b_deficiencies
Saturday, February 21, 2009
Education protects against pre-Alzheimer's memory loss
nother study has come out supporting the view that people with more education and more mentally demanding occupations may have protection againhe memory loss that precedes Alzheimer's disease, providing more evidence for the idea of cognitive reserve. The 14-month study followed 242 people with Alzheimer's disease, 72 people with mild cognitive impairment, and 144 people with no memory problems. During the study period, 21 of the people with MCI developed Alzheimer's. The metabolic changes in those with MCI who developed Alzheimer’s indicate the cognitive reserve is already in play in the pre-dementia stage.
The study was published in the October 21 issue of Neurology. Full reference
http://www.eurekalert.org/pub_releases/2008-10/aaon-epa101408.php
The study was published in the October 21 issue of Neurology. Full reference
http://www.eurekalert.org/pub_releases/2008-10/aaon-epa101408.php
MRI brain scans accurate in early diagnosis of Alzheimer's disease
Adding to the growing body of evidence indicating MRI brain scans provide valuable diagnostic information about Alzheimer's disease, a study in which a new visual rating system for evaluating the severity of shrinkage in the medial temporal lobe was used on brain scans of 260 people has found that scores accurately distinguished those with Alzheimer’s from those with mild cognitive impairment and those without memory problems. The test also accurately predicted those who would move from one group to another within a year or two.
The study was reported in the December issue of Neurology. Full reference
http://www.eurekalert.org/pub_releases/2008-12/uosf-mb
The study was reported in the December issue of Neurology. Full reference
http://www.eurekalert.org/pub_releases/2008-12/uosf-mb
UC Irvine starts clinical trial on nicotinamide effect in Alzheimer’s patients
Irvine, Calif., November 4, 2008
An over-the-counter vitamin in high doses prevented memory loss in mice with Alzheimer’s disease, and UC Irvine scientists now are conducting a clinical trial to determine its effect in humans.
Nicotinamide, a form of vitamin B3, lowered levels of a protein called phosphorylated tau that leads to the development of tangles, one of two brain lesions associated with Alzheimer’s disease. The vitamin also strengthened scaffolding along which information travels in brain cells, helping to keep neurons alive and further preventing symptoms in mice genetically wired to develop Alzheimer’s.
“Nicotinamide has a very robust effect on neurons,” said Kim Green, UCI scientist and lead author of the study. “Nicotinamide prevents loss of cognition in mice with Alzheimer’s disease, and the beauty of it is we already are moving forward with a clinical trial.”
The study appears online Nov. 5 in the Journal of Neuroscience.
Nicotinamide is a water-soluble vitamin sold in health food stores. It generally is safe but can be toxic in very high doses. Clinical trials have shown it benefits people with diabetes complications and has anti-inflammatory properties that may help people with skin conditions.
Nicotinamide belongs to a class of compounds called HDAC inhibitors, which have been shown to protect the central nervous system in rodent models of Parkinson’s and Huntington’s diseases and amyotrophic lateral sclerosis. Clinical trials are underway to learn whether HDAC inhibitors help ALS and Huntington’s patients.
In the nicotinamide study, Green and his colleague, Frank LaFerla, added the vitamin to drinking water fed to mice. They tested the rodents’ short-term and long-term memory over time using water-maze and object-recognition tasks and found that treated Alzheimer’s mice performed at the same level as normal mice, while untreated Alzheimer’s mice experienced memory loss.
The nicotinamide, in fact, slightly enhanced cognitive abilities in normal mice. “This suggests that not only is it good for Alzheimer’s disease, but if normal people take it, some aspects of their memory might improve,” said LaFerla, UCI neurobiology and behavior professor.
Scientists also found that the nicotinamide-treated animals had dramatically lower levels of the tau protein that leads to the Alzheimer’s tangle lesion. The vitamin did not affect levels of the protein beta amyloid, which clumps in the brain to form plaques, the second type of Alzheimer’s lesion.
Nicotinamide, they found, led to an increase in proteins that strengthen microtubules, the scaffolding within brain cells along which information travels. When this scaffolding breaks down, the brain cells can die. Neuronal death leads to dementia experienced by Alzheimer’s patients.
“Microtubules are like highways inside cells. What we’re doing with nicotinamide is making a wider, more stable highway,” Green said. “In Alzheimer’s disease, this highway breaks down. We are preventing that from happening.”
LaFerla and Green are affiliated with the Institute for Brain Aging and Dementia, which is conducting the clinical trial with funding from the Alzheimer’s Association.
The institute seeks volunteers who have been diagnosed with Alzheimer’s, are 50 or older, and have a friend or relative who can accompany them to clinic visits and answer questions. Study participants will take the vitamin supplement or a placebo twice daily for 24 weeks, with seven visits to the UCI clinic.
For more information on the clinical trial, contact Beatriz Yanez at 949-824-5733.
UCI scientists Joan Steffan, Hilda Martinez-Coria, Xuemin Sun, Steven Schreiber and Leslie Thompson also worked on the study, which was supported in part by the Alzheimer’s Drug Discovery Foundation and the National Institutes of Health.
http://www.today.uci.edu/news/release_detail.asp?key=1849
An over-the-counter vitamin in high doses prevented memory loss in mice with Alzheimer’s disease, and UC Irvine scientists now are conducting a clinical trial to determine its effect in humans.
Nicotinamide, a form of vitamin B3, lowered levels of a protein called phosphorylated tau that leads to the development of tangles, one of two brain lesions associated with Alzheimer’s disease. The vitamin also strengthened scaffolding along which information travels in brain cells, helping to keep neurons alive and further preventing symptoms in mice genetically wired to develop Alzheimer’s.
“Nicotinamide has a very robust effect on neurons,” said Kim Green, UCI scientist and lead author of the study. “Nicotinamide prevents loss of cognition in mice with Alzheimer’s disease, and the beauty of it is we already are moving forward with a clinical trial.”
The study appears online Nov. 5 in the Journal of Neuroscience.
Nicotinamide is a water-soluble vitamin sold in health food stores. It generally is safe but can be toxic in very high doses. Clinical trials have shown it benefits people with diabetes complications and has anti-inflammatory properties that may help people with skin conditions.
Nicotinamide belongs to a class of compounds called HDAC inhibitors, which have been shown to protect the central nervous system in rodent models of Parkinson’s and Huntington’s diseases and amyotrophic lateral sclerosis. Clinical trials are underway to learn whether HDAC inhibitors help ALS and Huntington’s patients.
In the nicotinamide study, Green and his colleague, Frank LaFerla, added the vitamin to drinking water fed to mice. They tested the rodents’ short-term and long-term memory over time using water-maze and object-recognition tasks and found that treated Alzheimer’s mice performed at the same level as normal mice, while untreated Alzheimer’s mice experienced memory loss.
The nicotinamide, in fact, slightly enhanced cognitive abilities in normal mice. “This suggests that not only is it good for Alzheimer’s disease, but if normal people take it, some aspects of their memory might improve,” said LaFerla, UCI neurobiology and behavior professor.
Scientists also found that the nicotinamide-treated animals had dramatically lower levels of the tau protein that leads to the Alzheimer’s tangle lesion. The vitamin did not affect levels of the protein beta amyloid, which clumps in the brain to form plaques, the second type of Alzheimer’s lesion.
Nicotinamide, they found, led to an increase in proteins that strengthen microtubules, the scaffolding within brain cells along which information travels. When this scaffolding breaks down, the brain cells can die. Neuronal death leads to dementia experienced by Alzheimer’s patients.
“Microtubules are like highways inside cells. What we’re doing with nicotinamide is making a wider, more stable highway,” Green said. “In Alzheimer’s disease, this highway breaks down. We are preventing that from happening.”
LaFerla and Green are affiliated with the Institute for Brain Aging and Dementia, which is conducting the clinical trial with funding from the Alzheimer’s Association.
The institute seeks volunteers who have been diagnosed with Alzheimer’s, are 50 or older, and have a friend or relative who can accompany them to clinic visits and answer questions. Study participants will take the vitamin supplement or a placebo twice daily for 24 weeks, with seven visits to the UCI clinic.
For more information on the clinical trial, contact Beatriz Yanez at 949-824-5733.
UCI scientists Joan Steffan, Hilda Martinez-Coria, Xuemin Sun, Steven Schreiber and Leslie Thompson also worked on the study, which was supported in part by the Alzheimer’s Drug Discovery Foundation and the National Institutes of Health.
http://www.today.uci.edu/news/release_detail.asp?key=1849
Vitamin B3 (niacin) review
• Basics: water-soluble vitamin, nicotinic acid, nicotinamide, niacinamide and antipellagra vitamin; essential in the metabolism of carbohydrates (to produce energy), fats, and proteins. • Benefits: facilitates the body's ability to eliminate toxins, assists in antioxidant and detoxification functions, helps stabilize blood sugar, relieves acne, migraines, vertigo, forgetfulness, high blood pressure and diarrhea. • Dosage: 19 mg per day for adult males and 13 mg per day for adult females, doses should be divided into 2-3 separate daily doses. • Sources: brewer's yeast, broccoli, carrots, cheese, corn flour, dandelion greens, dates, eggs, fish, milk, peanuts, pork, potatoes, tomatoes, beef liver, beef kidney, veal, fish, salmon, swordfish, tuna, sunflower seeds, and peanuts. • Deficiency: pellagra is a disease caused by niacin deficiency, characterized by mouth sores, skin rashes, diarrhea, and dementia. • Overdose: high doses of niacin causes liver damage, peptic ulcers, and skin rashes, nicotinic acid overdose causes skin flushing, headaches, low blood pressure.
Vitamin B3 (niacin, nicotinic acid, nicotinamide, niacinamide)
Vitamin B3 is also known as niacin, nicotinic acid, nicotinamide, niacinamide and antipellagra vitamin or PP factor. Niacin is a water-soluble vitamin whose derivatives such as NADH play essential roles in energy metabolism in the living cell. Niacin works closely with vitamin B1, vitamin B2, vitamin B6, pantothenic acid, and biotin to break the carbohydrates, fats, and proteins in food
down into energy. Vitamin B3 is essential in the metabolism of carbohydrates (to produce energy), fats, and proteins. It also aids in the production of hydrochloric acid, needed for proper digestion. Additionally, vitamin B3 facilitates the body's ability to eliminate toxins. The name niacin derives from nicotinic acid + in. When the properties of niacin were discovered, it was thought prudent to choose a common name other than nicotinic acid, for fear that it might be confused with nicotine, leading to the ideas that either smoking provided vitamins or that wholesome food contained a poison.
Niacin plays an important role in ridding the body of toxic and harmful chemicals. It also helps the body make various sex and stress-related hormones in the adrenal glands and other parts of the body. Vitamin B3 is essential for the activity of many enzymes in the body. Enzymes are special substances that speed up chemical reactions in the body. These enzymes are responsible for the production of energy in the body, the breakdown of dietary fats, the production of certain hormones and cholesterol, the processing of genetic material (DNA) and the growth and maturation of the cells in the body. Niacin is effective in improving circulation and reducing cholesterol levels in the blood. Niacin needs can be partially met by eating foods containing protein because the human body is able to convert tryptophan, an amino acid, into niacin. Niacin, via its metabolites, is involved in a wide range of biological processes, including the production of energy, the synthesis of fatty acids, cholesterol and steroids, signal transduction, the regulation of gene expression and the maintenance of genomic integrity. Nicotinic acid, in pharmacological doses, is used as an antihyperlipidemic agent. Niacinamide is used to treat osteoarthritis, rheumatoid arthritis, insomnia, migraine headaches, and insulin-dependent diabetes. Vitamin B3 (Niacin) increases good cholesterol (HDL) and lowers bad cholesterol (LDL). Niacin may enhance the effectiveness of some medications prescribed to lower cholesterol.
Vitamin B3 comes in two basic forms - niacin (also called nicotinic acid) and niacinamide (also called nicotinamide). A variation on niacin, called inositol hexaniacinate, is also available in supplements. Niacin can be found in nuts, dairy products, lean meats, poultry, fish, and eggs. Some niacin is also supplied by legumes and enriched breads and cereals. The best dietary sources of vitamin B3 are found in beets, brewer's yeast, beef liver, beef kidney, pork, turkey, chicken, veal, fish, salmon, swordfish, tuna, sunflower seeds, and peanuts. The body can synthesize niacin from the essential amino acid tryptophan, but the synthesis is extremely slow; 60 mg of tryptophan are required to make one milligram of niacin. For this reason, eating lots of tryptophan is not an adequate substitute for consuming niacin. As serotonin synthesis is reliant on tryptophan availability, inadequate dietary intake of vitamin B3 may also therefore lead to depression. The liver is the main storage area for this vitamin and absorption of vitamin B3 takes place in the intestines. Vitamin B3 is required by the body for digestive processes, activating enzymes which nourish the brain, regulating blood pressure and regulating cholesterol levels.
http://www.vitamins-supplements.org/vitamin-B3-niacin.php
down into energy. Vitamin B3 is essential in the metabolism of carbohydrates (to produce energy), fats, and proteins. It also aids in the production of hydrochloric acid, needed for proper digestion. Additionally, vitamin B3 facilitates the body's ability to eliminate toxins. The name niacin derives from nicotinic acid + in. When the properties of niacin were discovered, it was thought prudent to choose a common name other than nicotinic acid, for fear that it might be confused with nicotine, leading to the ideas that either smoking provided vitamins or that wholesome food contained a poison.
Niacin plays an important role in ridding the body of toxic and harmful chemicals. It also helps the body make various sex and stress-related hormones in the adrenal glands and other parts of the body. Vitamin B3 is essential for the activity of many enzymes in the body. Enzymes are special substances that speed up chemical reactions in the body. These enzymes are responsible for the production of energy in the body, the breakdown of dietary fats, the production of certain hormones and cholesterol, the processing of genetic material (DNA) and the growth and maturation of the cells in the body. Niacin is effective in improving circulation and reducing cholesterol levels in the blood. Niacin needs can be partially met by eating foods containing protein because the human body is able to convert tryptophan, an amino acid, into niacin. Niacin, via its metabolites, is involved in a wide range of biological processes, including the production of energy, the synthesis of fatty acids, cholesterol and steroids, signal transduction, the regulation of gene expression and the maintenance of genomic integrity. Nicotinic acid, in pharmacological doses, is used as an antihyperlipidemic agent. Niacinamide is used to treat osteoarthritis, rheumatoid arthritis, insomnia, migraine headaches, and insulin-dependent diabetes. Vitamin B3 (Niacin) increases good cholesterol (HDL) and lowers bad cholesterol (LDL). Niacin may enhance the effectiveness of some medications prescribed to lower cholesterol.
Vitamin B3 comes in two basic forms - niacin (also called nicotinic acid) and niacinamide (also called nicotinamide). A variation on niacin, called inositol hexaniacinate, is also available in supplements. Niacin can be found in nuts, dairy products, lean meats, poultry, fish, and eggs. Some niacin is also supplied by legumes and enriched breads and cereals. The best dietary sources of vitamin B3 are found in beets, brewer's yeast, beef liver, beef kidney, pork, turkey, chicken, veal, fish, salmon, swordfish, tuna, sunflower seeds, and peanuts. The body can synthesize niacin from the essential amino acid tryptophan, but the synthesis is extremely slow; 60 mg of tryptophan are required to make one milligram of niacin. For this reason, eating lots of tryptophan is not an adequate substitute for consuming niacin. As serotonin synthesis is reliant on tryptophan availability, inadequate dietary intake of vitamin B3 may also therefore lead to depression. The liver is the main storage area for this vitamin and absorption of vitamin B3 takes place in the intestines. Vitamin B3 is required by the body for digestive processes, activating enzymes which nourish the brain, regulating blood pressure and regulating cholesterol levels.
http://www.vitamins-supplements.org/vitamin-B3-niacin.php
Wednesday, February 18, 2009
Vitamin B3 reduces Alzheimer's symptoms, lesions - UC Irvine starts clinical trial on nicotinamide effect in Alzheimer’s patients
Vitamin B3 reduces Alzheimer's symptoms, lesions
UC Irvine starts clinical trial on nicotinamide effect in Alzheimer’s patients
Irvine, Calif., November 4, 2008
An over-the-counter vitamin in high doses prevented memory loss in mice with Alzheimer’s disease, and UC Irvine scientists now are conducting a clinical trial to determine its effect in humans.
Nicotinamide, a form of vitamin B3, lowered levels of a protein called phosphorylated tau that leads to the development of tangles, one of two brain lesions associated with Alzheimer’s disease. The vitamin also strengthened scaffolding along which information travels in brain cells, helping to keep neurons alive and further preventing symptoms in mice genetically wired to develop Alzheimer’s.
“Nicotinamide has a very robust effect on neurons,” said Kim Green, UCI scientist and lead author of the study. “Nicotinamide prevents loss of cognition in mice with Alzheimer’s disease, and the beauty of it is we already are moving forward with a clinical trial.”
The study appears online Nov. 5 in the Journal of Neuroscience.
Nicotinamide is a water-soluble vitamin sold in health food stores. It generally is safe but can be toxic in very high doses. Clinical trials have shown it benefits people with diabetes complications and has anti-inflammatory properties that may help people with skin conditions.
Nicotinamide belongs to a class of compounds called HDAC inhibitors, which have been shown to protect the central nervous system in rodent models of Parkinson’s and Huntington’s diseases and amyotrophic lateral sclerosis. Clinical trials are underway to learn whether HDAC inhibitors help ALS and Huntington’s patients.
In the nicotinamide study, Green and his colleague, Frank LaFerla, added the vitamin to drinking water fed to mice. They tested the rodents’ short-term and long-term memory over time using water-maze and object-recognition tasks and found that treated Alzheimer’s mice performed at the same level as normal mice, while untreated Alzheimer’s mice experienced memory loss.
The nicotinamide, in fact, slightly enhanced cognitive abilities in normal mice. “This suggests that not only is it good for Alzheimer’s disease, but if normal people take it, some aspects of their memory might improve,” said LaFerla, UCI neurobiology and behavior professor.
Scientists also found that the nicotinamide-treated animals had dramatically lower levels of the tau protein that leads to the Alzheimer’s tangle lesion. The vitamin did not affect levels of the protein beta amyloid, which clumps in the brain to form plaques, the second type of Alzheimer’s lesion.
Nicotinamide, they found, led to an increase in proteins that strengthen microtubules, the scaffolding within brain cells along which information travels. When this scaffolding breaks down, the brain cells can die. Neuronal death leads to dementia experienced by Alzheimer’s patients.
“Microtubules are like highways inside cells. What we’re doing with nicotinamide is making a wider, more stable highway,” Green said. “In Alzheimer’s disease, this highway breaks down. We are preventing that from happening.”
LaFerla and Green are affiliated with the Institute for Brain Aging and Dementia, which is conducting the clinical trial with funding from the Alzheimer’s Association.
The institute seeks volunteers who have been diagnosed with Alzheimer’s, are 50 or older, and have a friend or relative who can accompany them to clinic visits and answer questions. Study participants will take the vitamin supplement or a placebo twice daily for 24 weeks, with seven visits to the UCI clinic.
For more information on the clinical trial, contact Beatriz Yanez at 949-824-5733.
UCI scientists Joan Steffan, Hilda Martinez-Coria, Xuemin Sun, Steven Schreiber and Leslie Thompson also worked on the study, which was supported in part by the Alzheimer’s Drug Discovery Foundation and the National Institutes of Health.
http://today.uci.edu/NEWS/release_detail.asp?key=1849
UC Irvine starts clinical trial on nicotinamide effect in Alzheimer’s patients
Irvine, Calif., November 4, 2008
An over-the-counter vitamin in high doses prevented memory loss in mice with Alzheimer’s disease, and UC Irvine scientists now are conducting a clinical trial to determine its effect in humans.
Nicotinamide, a form of vitamin B3, lowered levels of a protein called phosphorylated tau that leads to the development of tangles, one of two brain lesions associated with Alzheimer’s disease. The vitamin also strengthened scaffolding along which information travels in brain cells, helping to keep neurons alive and further preventing symptoms in mice genetically wired to develop Alzheimer’s.
“Nicotinamide has a very robust effect on neurons,” said Kim Green, UCI scientist and lead author of the study. “Nicotinamide prevents loss of cognition in mice with Alzheimer’s disease, and the beauty of it is we already are moving forward with a clinical trial.”
The study appears online Nov. 5 in the Journal of Neuroscience.
Nicotinamide is a water-soluble vitamin sold in health food stores. It generally is safe but can be toxic in very high doses. Clinical trials have shown it benefits people with diabetes complications and has anti-inflammatory properties that may help people with skin conditions.
Nicotinamide belongs to a class of compounds called HDAC inhibitors, which have been shown to protect the central nervous system in rodent models of Parkinson’s and Huntington’s diseases and amyotrophic lateral sclerosis. Clinical trials are underway to learn whether HDAC inhibitors help ALS and Huntington’s patients.
In the nicotinamide study, Green and his colleague, Frank LaFerla, added the vitamin to drinking water fed to mice. They tested the rodents’ short-term and long-term memory over time using water-maze and object-recognition tasks and found that treated Alzheimer’s mice performed at the same level as normal mice, while untreated Alzheimer’s mice experienced memory loss.
The nicotinamide, in fact, slightly enhanced cognitive abilities in normal mice. “This suggests that not only is it good for Alzheimer’s disease, but if normal people take it, some aspects of their memory might improve,” said LaFerla, UCI neurobiology and behavior professor.
Scientists also found that the nicotinamide-treated animals had dramatically lower levels of the tau protein that leads to the Alzheimer’s tangle lesion. The vitamin did not affect levels of the protein beta amyloid, which clumps in the brain to form plaques, the second type of Alzheimer’s lesion.
Nicotinamide, they found, led to an increase in proteins that strengthen microtubules, the scaffolding within brain cells along which information travels. When this scaffolding breaks down, the brain cells can die. Neuronal death leads to dementia experienced by Alzheimer’s patients.
“Microtubules are like highways inside cells. What we’re doing with nicotinamide is making a wider, more stable highway,” Green said. “In Alzheimer’s disease, this highway breaks down. We are preventing that from happening.”
LaFerla and Green are affiliated with the Institute for Brain Aging and Dementia, which is conducting the clinical trial with funding from the Alzheimer’s Association.
The institute seeks volunteers who have been diagnosed with Alzheimer’s, are 50 or older, and have a friend or relative who can accompany them to clinic visits and answer questions. Study participants will take the vitamin supplement or a placebo twice daily for 24 weeks, with seven visits to the UCI clinic.
For more information on the clinical trial, contact Beatriz Yanez at 949-824-5733.
UCI scientists Joan Steffan, Hilda Martinez-Coria, Xuemin Sun, Steven Schreiber and Leslie Thompson also worked on the study, which was supported in part by the Alzheimer’s Drug Discovery Foundation and the National Institutes of Health.
http://today.uci.edu/NEWS/release_detail.asp?key=1849
Monday, February 16, 2009
Vitamin 'may be Alzheimer's aid'
A vitamin found in meat, fish and potatoes may help protect the brain from Alzheimer's disease - and even boost memory in healthy people.
US researchers found vitamin B3 lowered levels of a protein linked to Alzheimer's damage in mice.
The Journal of Neuroscience study also showed the animals performed better at memory tests.
UK Alzheimer's charities said people should not start taking the vitamin before results from human studies.
This suggests that not only is it good for Alzheimer's disease, but if normal people take it, some aspects of their memory might improve
Professor Frank LaFerla
University of California, Irvine
The vitamin, also called nicotinamide by scientists, is sold in UK pharmacies and health food shops.
It has already been shown to help people suffering from diabetes complications and has some anti-inflammatory qualities.
The researchers, from the University of California at Irvine, added the vitamin to drinking water given to mice bred to develop a version of Alzheimer's disease, then tested the levels of certain chemicals associated with the condition.
They found that levels of one, called phosphorylated tau, were significantly lower in the animals.
This protein is involved in abnormal 'deposits' in brain cells, called 'tangles', which contribute to the brain damage which progressively affects people with Alzheimer's.
Using 'water mazes', the team also found some evidence that memory was enhanced in both 'Alzheimer's' mice and unaffected mice.
Normal memory
Dr Kim Green, who led the study, said that human tests were progressing: "Nicotinamide has a very robust effect on neurons. It prevents loss of cognition in mice with Alzheimer's disease, and the beauty of it is we already are moving forward with a clinical trial."
His colleague Professor Frank LaFerla, said: "This suggests that not only is it good for Alzheimer's disease, but if normal people take it, some aspects of their memory might improve."
Susanne Sorensen, the head of research at the Alzheimer's Society, said the research was "interesting" and pointed to new ways to treat the condition.
"From the research, it appears that Nicotinamide has more than one beneficial effect on nerve cells including the facilitation of the recycling of the 'bad' phosphorylated tau.
"Nicotinamide occurs naturally in meat, fish, beans, cereals and potatoes and is cheap and easy to take.
"However, more research is now needed to explore the possible mechanisms involved so we can better understand if Nicotinamide could have the same effect in people and, if it does, what level of vitamin intake would be required."
Rebecca Wood, Chief Executive of the Alzheimer's Research Trust, said until the human research was completed, people should not start taking the supplement.
"These are exciting findings, but until the results from the human clinical trial are announced, people should be wary about changing their diet or taking supplements. In high doses vitamin B3 can be toxic."
http://news.bbc.co.uk/2/hi/health/7710365.stm
US researchers found vitamin B3 lowered levels of a protein linked to Alzheimer's damage in mice.
The Journal of Neuroscience study also showed the animals performed better at memory tests.
UK Alzheimer's charities said people should not start taking the vitamin before results from human studies.
This suggests that not only is it good for Alzheimer's disease, but if normal people take it, some aspects of their memory might improve
Professor Frank LaFerla
University of California, Irvine
The vitamin, also called nicotinamide by scientists, is sold in UK pharmacies and health food shops.
It has already been shown to help people suffering from diabetes complications and has some anti-inflammatory qualities.
The researchers, from the University of California at Irvine, added the vitamin to drinking water given to mice bred to develop a version of Alzheimer's disease, then tested the levels of certain chemicals associated with the condition.
They found that levels of one, called phosphorylated tau, were significantly lower in the animals.
This protein is involved in abnormal 'deposits' in brain cells, called 'tangles', which contribute to the brain damage which progressively affects people with Alzheimer's.
Using 'water mazes', the team also found some evidence that memory was enhanced in both 'Alzheimer's' mice and unaffected mice.
Normal memory
Dr Kim Green, who led the study, said that human tests were progressing: "Nicotinamide has a very robust effect on neurons. It prevents loss of cognition in mice with Alzheimer's disease, and the beauty of it is we already are moving forward with a clinical trial."
His colleague Professor Frank LaFerla, said: "This suggests that not only is it good for Alzheimer's disease, but if normal people take it, some aspects of their memory might improve."
Susanne Sorensen, the head of research at the Alzheimer's Society, said the research was "interesting" and pointed to new ways to treat the condition.
"From the research, it appears that Nicotinamide has more than one beneficial effect on nerve cells including the facilitation of the recycling of the 'bad' phosphorylated tau.
"Nicotinamide occurs naturally in meat, fish, beans, cereals and potatoes and is cheap and easy to take.
"However, more research is now needed to explore the possible mechanisms involved so we can better understand if Nicotinamide could have the same effect in people and, if it does, what level of vitamin intake would be required."
Rebecca Wood, Chief Executive of the Alzheimer's Research Trust, said until the human research was completed, people should not start taking the supplement.
"These are exciting findings, but until the results from the human clinical trial are announced, people should be wary about changing their diet or taking supplements. In high doses vitamin B3 can be toxic."
http://news.bbc.co.uk/2/hi/health/7710365.stm
Vitamin B3 Reduces Alzheimer's Symptoms
Vitamin B3 Reduces Alzheimer's Symptoms, Lesions: Clinical Trial On Nicotinamide Effect In Alzheimer's Patients
ScienceDaily (Nov. 5, 2008) — An over-the-counter vitamin in high doses prevented memory loss in mice with Alzheimer's disease, and UC Irvine scientists now are conducting a clinical trial to determine its effect in humans.
Nicotinamide, a form of vitamin B3, lowered levels of a protein called phosphorylated tau that leads to the development of tangles, one of two brain lesions associated with Alzheimer's disease. The vitamin also strengthened scaffolding along which information travels in brain cells, helping to keep neurons alive and further preventing symptoms in mice genetically wired to develop Alzheimer's.
"Nicotinamide has a very robust effect on neurons," said Kim Green, UCI scientist and lead author of the study. "Nicotinamide prevents loss of cognition in mice with Alzheimer's disease, and the beauty of it is we already are moving forward with a clinical trial."
The study appears online Nov. 5 in the Journal of Neuroscience.
Nicotinamide is a water-soluble vitamin sold in health food stores. It generally is safe but can be toxic in very high doses. Clinical trials have shown it benefits people with diabetes complications and has anti-inflammatory properties that may help people with skin conditions.
Nicotinamide belongs to a class of compounds called HDAC inhibitors, which have been shown to protect the central nervous system in rodent models of Parkinson's and Huntington's diseases and amyotrophic lateral sclerosis. Clinical trials are underway to learn whether HDAC inhibitors help ALS and Huntington's patients.
In the nicotinamide study, Green and his colleague, Frank LaFerla, added the vitamin to drinking water fed to mice. They tested the rodents' short-term and long-term memory over time using water-maze and object-recognition tasks and found that treated Alzheimer's mice performed at the same level as normal mice, while untreated Alzheimer's mice experienced memory loss.
The nicotinamide, in fact, slightly enhanced cognitive abilities in normal mice. "This suggests that not only is it good for Alzheimer's disease, but if normal people take it, some aspects of their memory might improve," said LaFerla, UCI neurobiology and behavior professor.
Scientists also found that the nicotinamide-treated animals had dramatically lower levels of the tau protein that leads to the Alzheimer's tangle lesion. The vitamin did not affect levels of the protein beta amyloid, which clumps in the brain to form plaques, the second type of Alzheimer's lesion.
Nicotinamide, they found, led to an increase in proteins that strengthen microtubules, the scaffolding within brain cells along which information travels. When this scaffolding breaks down, the brain cells can die. Neuronal death leads to dementia experienced by Alzheimer's patients.
"Microtubules are like highways inside cells. What we're doing with nicotinamide is making a wider, more stable highway," Green said. "In Alzheimer's disease, this highway breaks down. We are preventing that from happening."
Vitamin B3 Reduces Alzheimer's Symptoms http://www.sciencedaily.com/releases/2008/11/081104180926.htm
ScienceDaily (Nov. 5, 2008) — An over-the-counter vitamin in high doses prevented memory loss in mice with Alzheimer's disease, and UC Irvine scientists now are conducting a clinical trial to determine its effect in humans.
Nicotinamide, a form of vitamin B3, lowered levels of a protein called phosphorylated tau that leads to the development of tangles, one of two brain lesions associated with Alzheimer's disease. The vitamin also strengthened scaffolding along which information travels in brain cells, helping to keep neurons alive and further preventing symptoms in mice genetically wired to develop Alzheimer's.
"Nicotinamide has a very robust effect on neurons," said Kim Green, UCI scientist and lead author of the study. "Nicotinamide prevents loss of cognition in mice with Alzheimer's disease, and the beauty of it is we already are moving forward with a clinical trial."
The study appears online Nov. 5 in the Journal of Neuroscience.
Nicotinamide is a water-soluble vitamin sold in health food stores. It generally is safe but can be toxic in very high doses. Clinical trials have shown it benefits people with diabetes complications and has anti-inflammatory properties that may help people with skin conditions.
Nicotinamide belongs to a class of compounds called HDAC inhibitors, which have been shown to protect the central nervous system in rodent models of Parkinson's and Huntington's diseases and amyotrophic lateral sclerosis. Clinical trials are underway to learn whether HDAC inhibitors help ALS and Huntington's patients.
In the nicotinamide study, Green and his colleague, Frank LaFerla, added the vitamin to drinking water fed to mice. They tested the rodents' short-term and long-term memory over time using water-maze and object-recognition tasks and found that treated Alzheimer's mice performed at the same level as normal mice, while untreated Alzheimer's mice experienced memory loss.
The nicotinamide, in fact, slightly enhanced cognitive abilities in normal mice. "This suggests that not only is it good for Alzheimer's disease, but if normal people take it, some aspects of their memory might improve," said LaFerla, UCI neurobiology and behavior professor.
Scientists also found that the nicotinamide-treated animals had dramatically lower levels of the tau protein that leads to the Alzheimer's tangle lesion. The vitamin did not affect levels of the protein beta amyloid, which clumps in the brain to form plaques, the second type of Alzheimer's lesion.
Nicotinamide, they found, led to an increase in proteins that strengthen microtubules, the scaffolding within brain cells along which information travels. When this scaffolding breaks down, the brain cells can die. Neuronal death leads to dementia experienced by Alzheimer's patients.
"Microtubules are like highways inside cells. What we're doing with nicotinamide is making a wider, more stable highway," Green said. "In Alzheimer's disease, this highway breaks down. We are preventing that from happening."
Vitamin B3 Reduces Alzheimer's Symptoms http://www.sciencedaily.com/releases/2008/11/081104180926.htm
Sunday, September 28, 2008
What is Alzheimer's
Introduction
Alzheimer’s disease is a brain disorder named for German physician Alois Alzheimer, who first described it in 1906. Scientists have learned a great deal about Alzheimer’s disease in the century since Dr. Alzheimer first drew attention to it. Today we know that Alzheimer’s:
- Is a progressive and fatal brain disease
- Is the most common form of dementia
- Has no current cure
Alzheimer's and the brain
Just like the rest of our bodies, our brains change as we age. Most of us notice some slowed thinking and occasional problems remembering certain things. However, serious memory loss, confusion and other major changes in the way our minds work are not a normal part of aging. They may be a sign that brain cells are failing.
The role of plaques and tangles
Two abnormal structures called plaques and tangles are prime suspects in damaging and killing nerve cells. Plaques and tangles were among the abnormalities that Dr. Alois Alzheimer saw in the brain of Auguste D., although he called them different names.
More...
http://www.alz.org/alzheimers_disease_what_is_alzheimers.asp
Alzheimer’s disease is a brain disorder named for German physician Alois Alzheimer, who first described it in 1906. Scientists have learned a great deal about Alzheimer’s disease in the century since Dr. Alzheimer first drew attention to it. Today we know that Alzheimer’s:
- Is a progressive and fatal brain disease
- Is the most common form of dementia
- Has no current cure
Alzheimer's and the brain
Just like the rest of our bodies, our brains change as we age. Most of us notice some slowed thinking and occasional problems remembering certain things. However, serious memory loss, confusion and other major changes in the way our minds work are not a normal part of aging. They may be a sign that brain cells are failing.
The role of plaques and tangles
Two abnormal structures called plaques and tangles are prime suspects in damaging and killing nerve cells. Plaques and tangles were among the abnormalities that Dr. Alois Alzheimer saw in the brain of Auguste D., although he called them different names.
More...
http://www.alz.org/alzheimers_disease_what_is_alzheimers.asp
Stages of Alzheimer's
Experts have documented common patterns of symptom progression that occur in many individuals with Alzheimer’s disease and developed several methods of “staging” based on these patterns.
Staging systems provide useful frames of reference for understanding how the disease may unfold and for making future plans. But it is important to note that not everyone will experience the same symptoms or progress at the same rate. People with Alzheimer’s die an average of four to six years after diagnosis, but the duration of the disease can vary from three to 20 years.
The framework for this section is a system that outlines key symptoms characterizing seven stages ranging from unimpaired function to very severe cognitive decline. This framework is based on a system developed by Barry Reisberg, M.D., Clinical Director of the New York University School of Medicine’s Silberstein Aging and Dementia Research Center.
Within this framework, we have noted which stages correspond to the widely used concepts of mild, moderate, moderately severe and severe Alzheimer’s disease. We have also noted which stages fall within the more general divisions of early-stage, mid-stage and late-stage categories.
Stage 1:
No impairment (normal function)
Stage 2:
Very mild cognitive decline (may be normal age-related changes or earliest signs of Alzheimer's disease)
Stage 3:
Mild cognitive declineEarly-stage Alzheimer's can be diagnosed in some, but not all, individuals with these symptoms
Stage 4:
Moderate cognitive decline(Mild or early-stage Alzheimer's disease)
Stage 5:
Moderately severe cognitive decline(Moderate or mid-stage Alzheimer's disease)
Stage 6:
Severe cognitive decline(Moderately severe or mid-stage Alzheimer's disease)
Stage 7:
Very severe cognitive decline(Severe or late-stage Alzheimer's disease)
More...
http://www.alz.org/alzheimers_disease_stages_of_alzheimers.asp
Staging systems provide useful frames of reference for understanding how the disease may unfold and for making future plans. But it is important to note that not everyone will experience the same symptoms or progress at the same rate. People with Alzheimer’s die an average of four to six years after diagnosis, but the duration of the disease can vary from three to 20 years.
The framework for this section is a system that outlines key symptoms characterizing seven stages ranging from unimpaired function to very severe cognitive decline. This framework is based on a system developed by Barry Reisberg, M.D., Clinical Director of the New York University School of Medicine’s Silberstein Aging and Dementia Research Center.
Within this framework, we have noted which stages correspond to the widely used concepts of mild, moderate, moderately severe and severe Alzheimer’s disease. We have also noted which stages fall within the more general divisions of early-stage, mid-stage and late-stage categories.
Stage 1:
No impairment (normal function)
Stage 2:
Very mild cognitive decline (may be normal age-related changes or earliest signs of Alzheimer's disease)
Stage 3:
Mild cognitive declineEarly-stage Alzheimer's can be diagnosed in some, but not all, individuals with these symptoms
Stage 4:
Moderate cognitive decline(Mild or early-stage Alzheimer's disease)
Stage 5:
Moderately severe cognitive decline(Moderate or mid-stage Alzheimer's disease)
Stage 6:
Severe cognitive decline(Moderately severe or mid-stage Alzheimer's disease)
Stage 7:
Very severe cognitive decline(Severe or late-stage Alzheimer's disease)
More...
http://www.alz.org/alzheimers_disease_stages_of_alzheimers.asp
Saturday, September 27, 2008
Alzheimers's Disease
Symptoms
Memory loss is usually the first sign of Alzheimer's disease. Many older people may worry about Alzheimer's disease if they start to have memory problems. Having some short-term memory loss in your 60s and 70s is common, and some people with mild memory problems will go on to develop Alzheimer's disease. If you start having memory problems, share your concerns with your family and your doctor.
Examples of normal forgetfulness include forgetting:
Parts of an experience.
Where the car is parked.
Events from the distant past.
A person's name, remembering it later.
Where you left an object, such as your car keys.
Examples of memory loss caused by Alzheimer's disease include forgetting:
An entire experience.
How to drive a car or read a clock.
Recent events, such as forgetting you left the stove on.
Ever having known a particular person.
Alzheimer's disease also causes changes in thinking, behavior, and personality. Early in the disease, the person may still behave appropriately in social situations, leading others to believe that the person is not ill. Close family members and friends may first notice the symptoms of Alzheimer's disease, although the person may also realize that something is wrong.
Learn the warning signs of dementia—such as having difficulty thinking or remembering, or having trouble balancing a checkbook—and talk to a doctor if a friend or family member has developed any of the signs. Symptoms vary as the disease progresses.
More...
http://health.yahoo.com/alzheimers-symptoms/alzheimer-s-disease-symptoms/healthwise--hw136643.html
Memory loss is usually the first sign of Alzheimer's disease. Many older people may worry about Alzheimer's disease if they start to have memory problems. Having some short-term memory loss in your 60s and 70s is common, and some people with mild memory problems will go on to develop Alzheimer's disease. If you start having memory problems, share your concerns with your family and your doctor.
Examples of normal forgetfulness include forgetting:
Parts of an experience.
Where the car is parked.
Events from the distant past.
A person's name, remembering it later.
Where you left an object, such as your car keys.
Examples of memory loss caused by Alzheimer's disease include forgetting:
An entire experience.
How to drive a car or read a clock.
Recent events, such as forgetting you left the stove on.
Ever having known a particular person.
Alzheimer's disease also causes changes in thinking, behavior, and personality. Early in the disease, the person may still behave appropriately in social situations, leading others to believe that the person is not ill. Close family members and friends may first notice the symptoms of Alzheimer's disease, although the person may also realize that something is wrong.
Learn the warning signs of dementia—such as having difficulty thinking or remembering, or having trouble balancing a checkbook—and talk to a doctor if a friend or family member has developed any of the signs. Symptoms vary as the disease progresses.
More...
http://health.yahoo.com/alzheimers-symptoms/alzheimer-s-disease-symptoms/healthwise--hw136643.html
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