B Vitamins For Memory Loss And Dementia
Most attention on B vitamins for dementia focuses on vitamin B12, B6, and B9. This isnt surprising studies show that deficiencies in these vitamins are common in the elderly and can contribute to cognitive decline.
Treatment with a complex of B-vitamins helps to prevent neurodegeneration. One study showed that over two years, vitamin B treatment slowed shrinkage of the whole brain, and further study showed that B vitamins reduced gray matter atrophy in regions of the brain specifically susceptible to Alzheimers-related degeneration.
Other Potential Biologic Mechanisms Of Folate
Data are limited on potential mechanisms of folate effects on dementia other than homocysteine concentration. One possibility is that folate deficiency may decrease acetylcholine, a neurotransmitter that is reduced in Alzheimers disease. Folic acid is involved in the metabolic pathway for acetycholine synthesis. At least one animal model, however, did not find evidence of dietary folate effects on acetylcholine metabolism . Another possibility is that folate deficiency increases oxidative stress, but again, data on the antioxidant effects of folate are limited .
The Role Of Microglia In Alzheimers
Alzheimers disease is the most common form of dementia for which there is no effective treatment. Mounting evidence suggests that the accumulation and aggregation of amyloid- is a key initiating factor in a cascade of events that lead to Alzheimers disease. The Alzheimers brain is typified by a robust microglial immune response triggered by A accumulation. Furthermore, genetic studies have linked many immune genes subserving this microglial response to the risk of Alzheimers disease. Although microglia have emerged as an important player in Alzheimers disease development and progression, the role of these cells in the disease is complex and still not fully understood.
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Vitamin B3 And Alzheimer’s
A vitamin pill could slow the progression of Alzheimers disease, according to mediareports today. The Guardian said that animals studies found that nicotinamide, a form of vitamin B3, protected the animals from memory loss associated with a condition similar to Alzheimers.
But the dose used in the study – on mice – would be high if given at an equivalent level in humans, far higher than levels of the vitamin found in food or in vitamin supplements.
Vitamin B3, also known as niacin or nicotinic acid, can be found in low doses in foods such as meat, poultry, fish, nuts, beans and also in cereals and potatoes. It can also be obtained in vitamin supplements.
A human trial giving equivalent doses would have to use 2g of the vitamin a day. The Food Standards Agency advises that taking 500mg or less of nicotinamide supplements a day is unlikely to cause any harm, but that there is insufficient data to establish a safe upper level. The Guardian reports that serious side-effects, including liver damage, have been seen in doses of 10g or more.
At present, there is not enough evidence to advise taking vitamin B3 to treat Alzheimers.
Niacin And Alzheimersthe First Hints Of A Link
Niacin is an essential nutrient obtained from foods, such as fish, beef, chicken, and whole grains, and supplement sources. The vitamin, in its pharmacological form, is prescribed to increase high-density lipoprotein cholesterol, although its intake is not associated with a reduced risk of death, heart attack, or stroke.
A deficiency in niacin can cause pellagra, a condition that results in dementia . Since the 1980s, researchers have explored whether dietary niacin could help stave off some neurodegenerative diseases. A study conducted between 1993 and 2002 in a cohort of older adults in Chicago, for example, calculated niacin intake from dietary data on the participants food and supplement consumption. The team found that intake from both sources together was inversely associated with development of Alzheimers, and intake from food sources was also negatively associated with cognitive decline. A study published in 2017 also found a beneficial relationship between dietary intake of niacin in young adulthood and better cognitive function later in life.
These findings might not have been particularly persuasive, says Indiana University School of Medicine Alzheimers researcher Gary Landreth. But the existence of a potential link was provocative, he says. When Miguel Moutinho joined Landreths lab in 2016, the two decided to interrogate that link and see if it existed beyond the realm of epidemiological observation.
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Niacinamide Research On Mice
A 2008 study published in the Journal of Neuroscience with demented mice showed that treatment with niacinamide reversed Alzheimer’s by causing a 60% reduction in one of the Alzheimer markers and increasing the number of microtubules that carry information inside the brain cells .
A 2012 study on lab mice reported that niacinamide restored cognitive functioning and synaptic plasticity .
A 2013 study concluded that niacinamide prevented cognitive decline in Alzheimer’s mice through improved neuronal activity and reduced breakdown of brain tissue .
Jonathon V. Wright, M.D. reviewed 2008 studies on laboratory mice and concluded that there was no reason to wait for ‘more research’ before administering niacinamide to Alzheimer’s patients .
Nr Promotes Neuronal And Cognitive Health
Compared with the controls, the NR-treated mice had less of the protein tau in the brain, less DNA damage, and more neuroplasticity that is, the brains ability to rewire itself when it learns new things, stores new memories, or becomes damaged.
Additionally probably as a result of NRs ability to aid the self-renewal of stem cells, or cells that have the ability to transform into any other type of cell that the body needs the mice in the intervention group produced more neurons from neuronal stem cells.
Also, fewer neurons died or were damaged in these mice. Intriguingly, however, their levels of the beta-amyloid protein stayed the same as those of the control mice.
Finally, the researchers say that in the hippocampi a brain area involved in memory that often shrinks or is damaged in Alzheimers of the mice that received the treatment, NR appeared to get rid of the existing DNA damage or stop it from spreading.
All the brain changes were backed up by results from cognition and behavioral tests. All of the NR-treated mice performed better at maze tasks and object recognition tests, and they demonstrated stronger muscles and better gait.
Commenting on the results of the study, Dr. Richard J. Hodes director of the NIA says, The pursuit of interventions to prevent or delay Alzheimers and related dementias is an important national priority.
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Gene Silencing and Anti-Aging
Genes and gene therapy are proving to be a powerful tool in the latest frontier in the fight against aging. Genes are actually a small part of the DNA structure and cellular differentiation depends on not only gene expression but also on gene silencing. In other words, which genes are expressed determines the cell purpose and activity. Recent research has identified genes that influence longevity. In particular, a gene labeled, Sir2, for silent information regulator 2, has been shown to produce a protein, Sir2p, that extends cell life. Recent research has shown that Sir2p is a NAD-dependent histone deacetylase that connects metabolism, gene silencing, and cellular life extension . Niacinamide, by increasing NAD, enhances Sir2p activity.
Caloric restricted diets have long been known for their ability to extend the lifespan by slowing metabolism. NAD is essential in cellular metabolism. It was proposed by MIT researchers that by slowing metabolism NAD is spared, thereby enhancing Sir2p activity. Increasing intracellular NAD not only mimics the metabolic benefits of calorie restricted diets, but also helps maintain a balance of silent and active genes.
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Niacinamide and Diabetes
Niacinamide may also be of benefit in type II adult onset diabetes and chronic pancreatitis.
Niacinamides Other Diverse Benefits
Niacinamide: Benefits Uses And Side Effects
Niacinamide is one of the two forms of vitamin B3 the other being nicotinic acid. Vitamin B3 is also known as niacin.
Niacinamide and nicotinic acid both provide vitamin B3 activity, but they differ in chemical structure and how they affect your health.
This article explains what niacinamide is, its benefits, uses and potential side effects.
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Clinical Prospects For Niacin Use In Alzheimers And Other Neurodegenerative Diseases
University of Calgary neuroimmunologist Wee Yong, who did not participate in this study but peer-reviewed it, says that this is a very important work as the Alzheimers field has struggled for some time trying to find ways to remove amyloid- plaques. Niaspans effect on Alzheimers disease needs to be tested in humans, of course, but this is . . . ripe for clinical translation, he says.
This is the first time that a link between niacin and Alzheimers disease has been demonstrated in lab experiments. And recent studies by other teams, including Yongs, have reported similar effects of niacin in other neurological disorders. In 2020, Yong and his colleagues showed that niacin could enhance the phagocytic activity of microglia, specifically its ability to remove myelin debris in cultured cells and in a mouse model of multiple sclerosis. Treatment with niacin could rejuvenate . . . microglia to remove myelin debris and therefore to lead to improved myelin repair, says Yong. This protective effect was also mediated by the HCAR2 receptor.
Yong says his team came upon niacin by screening a library of more than one thousand generic medications, while looking for an agent that could stimulate myelin repair. According to Yong, he and his colleagues are trying to initiate a clinical trial to test niacin treatment for multiple sclerosis, but first they need to be more confident of the laboratory results.
Were pretty excited about this, concludes Landreth.
Niacin In The Central Nervous System
Besides dermatitis and diarrhea, niacin/tryptophan deficit symptoms also include several nervous system pathologies, such as dementia and depression, as well as other symptoms resembling those observed in neurodegenerative diseases. This evidence, together with accumulating in vitro and in vivo studies, has underlined the importance of niacin in growth and maintenance of the central nervous system .
Nicotinamide biosynthesis actively occurs in the mammalian brain, which contains nanomolar-low micromolar concentrations of nicotinamide precursors derived from the KP . Among them, quinolinic acid displays evident neuroactivity : it acts as a N-methyl-d-aspartate receptor agonist, thus causing excitotoxic neuronal lesions and oxidative stress . In addition, quinolinic acid concentrations in the brain positively correlate with age, thus contributing to neuron synapsis dropout occurring during aging . Finally, neuroinflammation, neurodegeneration and mood disturbs are accompanied by increased quinolinic acid levels in plasma and/or cerebrospinal fluid .
Beside the pro-differentiating action, nicotinamide also promotes neuronal survival, especially during oxidative stress conditions, and this effect is achieved via multiple mechanisms, including: prevention of cytochrome c release and caspase 3- and 9-like activities, inhibition of caspase-3-mediated degradation of forkhead transcription factor and maintenance of protein kinase B -dependent phosphorylation of FOXO3a .
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Protective Effects Of Nicotinamide As A Parp
Nicotinamide as a precursor of NAD+ has numerous important functions in cellular metabolism. Therefore, the supplementation of nicotinamide is relevant to the maintenance of NAD+ pools and their role as a cofactor of sirtuins, DNA repair, mitochondrial health and Ca+ homeostasis, autophagy of damaged cells all important in AD pathogenesis . In the following sections we discuss the potential additional role of nicotinamide as a PARP-1 inhibitor in the pathogenesis of AD through its role in cell death, mitochondrial function and inflammation.
Figure 1. Schematic representation of the proposed mechanisms of action of nicotinamide in the pathogenesis of Alzheimers disease. Red arrows indicate mechanisms of cellular damage in AD: pro-death, mitochondrial dysfunction and inflammation Blue arrows indicate protective effects of nicotinamide directly as a substrate for NAD+ synthesis with its effects on cellular metabolism, and through PARP-1 inhibition and its beneficial effects preventing cell death, mitochondrial dysfunction and inflammation. Other PARP-1 inhibitors may have similar effects.
Niacin Effectively Treats Alzheimers Mice
Since the increased dietary intake of niacin has been correlated with reduced Alzheimers risk, Moutinho and colleagues investigated how dietary intake of niacin reduced the risk of developing Alzheimers. Niacin is known to work by binding a receptor called HCAR2, which is expressed in the brain and has been shown to modulate microglial actions in several central nervous system disease models. Specifically, HCAR2 activation with niacin elicits several responses in microglial cells, including the secretion of inflammatory molecules and the monitoring and destruction of foreign substances. But not much has been known about whether HCAR2 modulation can affect microglial functions in Alzheimers.
Niacin stimulates microglia response and reduces amyloid pathology in Alzheimers mice.
Moutinho and colleagues report that the HCAR2 is required for efficient microglia proliferation, engagement with amyloid deposits, and engulfment of amyloid-, which are important microglial features reported to be beneficial in Alzheimers. Inactivating the HCAR2 gene in Alzheimers disease mice exacerbated cognitive impairments and amyloid- burden. These data provide direct evidence that HCAR2 is required for an efficient and neuroprotective response of microglia to amyloid pathology.
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Niacinamide: Niacins Sister Molecule Also Proposed As Treatment For Alzheimers
Niacinamide, also known as nicotinamide, is another form of vitamin B. Although the molecular structure of niacin and niacinamide differs, both play an essential role in the biosynthesis of NAD and its reduced form NADH, molecules involved in the synthesis of ATP, which cells use as a ready energy source.
Niacinamide has also been associated with protective effects in the central nervous system, although via different mechanisms than those described for niacin. For instance, in a mouse model of Alzheimers, niacinamide treatment reduced neuronal vulnerability to amyloid- toxicity and improved cognitive performance, mainly by enhancing brain bioenergetics. This form of vitamin B has also been reported to reduce a species of tau protein in a mouse model of Alzheimers. The body of research linking niacinamide with beneficial outcomes has motivated a few ongoing clinical trials, mainly in the US.
In an email, Indiana University School of Medicine researcher Miguel Moutinho explains that in the context of Alzheimers disease, in the brain . . . activation of HCAR2 is one of the main mechanisms through which nicotinic acid acts . . . while nicotinamide is probably more associated with production of NAD.
Clarification : The text has been updated to reflect David Morgan’s role with Biogen.
Caution Niacin Can Have Dangerous Interactions With Prescription Drugs
Niacin in large dosages is toxic and large amounts even in safe levels can also cause flushing. Also, niacin in large doses can lower blood cholesterol levels and can have dangerous interactions with other cholesterol lowering medications like statins. These interactions can lead to muscle damage and a very dangerous disease state that can damage kidneys called rhabdomyolysis. Too much niacin can also cause liver problems and lead to nausea, diarrhea and other gastrointestinal problems. Low blood pressure can also be a side effect from taking too much niacin and this can interact dangerously with blood pressure lowering medications. No one should take supplemental niacin without consulting a doctor, who can also monitor the effects of niacin with lab tests.
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Bottom Line On The Best Way To Take Niacinamide
If possible, taking 250 mg. every 90 minutes, 12 times a day seems to be the best method.
Sustained release niacinamide capsules are available on the internet and seem to be a reasonable compromise, though it is important to be aware that these doses are substantially above the Recommended Daily Allowances.
Caution: Niacin Can Have Dangerous Interactions With Prescription Drugs
This form of Vitamin B3 is found in Niacin, which in large dosages can be toxic. Also, niacin in large doses can lower blood cholesterol levels and can have dangerous interactions with other cholesterol lowering medications like statins. These interactions can lead to muscle damage and a very dangerous disease state that can damage kidneys called rhabdomyolysis. Too much niacin can also cause liver problems and lead to nausea, diarrhea and other gastrointestinal problems. Low blood pressure can also be a side effect from taking too much niacin and this can interact dangerously with blood pressure lowering medications.
No one should take supplemental niacin without consulting a doctor, who can also monitor the effects of niacin with lab tests.
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Niacinamide Treatment For Alzheimer’s
While many use the terms ‘Alzheimer’s disease’ and ‘dementia’ interchangeably, technically Alzheimer’s is one form of dementia and is the sixth leading cause of death in the U.S. Over 5 million Americans live with this disease, and one-third of seniors die with some form of dementia. The cost of treating Alzheimer’s is enormous. While the documented cost to the nation of treating Alzheimer’s in 2013 was over $203 billion, the unaccounted cost borne by family members was estimated to be over $216 billion in 2012.
This article examines whether niacinamide, which is a form of Vitamin B3, is helpful for symptoms relating to Alzheimer’s and Dementia, such as memory loss.
Someone in the U.S. develops Alzheimer’s every 68 seconds. Twice as many 70 year olds with Alzheimer’s die before they are 80, compared to 70 year olds who do not have Alzheimer’s. There is no way to prevent, cure or slow the progression of Alzheimer’s, though the quest for treating Alzheimer’s has spawned a sprawling, world-wide industry, supporting conferences, chains of nursing homes, expensive new drugs, on top of the ongoing costs of the physical care of patients.
Vitamin Pill That May Slow Alzheimer’s Goes On Trial
A vitamin pill that could slow the progression of Alzheimer’s disease is to enter human trials after scientists found it protected animals from memory loss associated with the condition.
High doses of vitamin B3 will be given to 70 people who have recently been diagnosed with the disease as part of the trial due to begin in the new year, which is open to volunteers over the age of 50.
If the six-month trial is a success it could have a dramatic impact on the treatment of an estimated 417,000 people in Britain who have been diagnosed with Alzheimer’s. There is currently no cure for Alzheimer’s or any other type of dementia.
Delaying the onset of the disease by five years would halve the number of deaths from the condition, saving 30,000 lives a year, according to the Alzheimer’s Society. Scientists at the University of California, Irvine, gave high doses of a form of vitamin B3 called nicotinamide to mice which had been genetically modified to develop Alzheimer’s disease. The researchers, led by Dr Kim Green, tested the animals’ memories over the four month study by seeing how well they remembered the location of a submerged platform in a large water tank.
“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 Frank LaFerla, a co-author on the study.