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    Home > Food News > Nutrition News > Can Vitamin Supplements Help Alzheimer's Patients?

    Can Vitamin Supplements Help Alzheimer's Patients?

    • Last Update: 2022-05-28
    • Source: Internet
    • Author: User
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    In 2020, nearly 6 million people in the United States had Alzheimer's disease, and this number is likely to increase in the coming decades
    .
    Attempts to develop drugs to treat the neurodegenerative disease have had limited success, with only six drugs currently approved by the FDA

    .
    The researchers also explored the potential of existing drugs to improve the condition of people with this type of dementia

    .
    Niacin, a form of vitamin B3, also known as niacin, has recently caught the attention of some researchers in the field

    .

    The vitamin has attracted interest over the past 20 years, with several epidemiological studies reporting a link between niacin intake and a reduced risk of overall cognitive decline
    .
    Recently, researchers have begun to explore whether the compound has a positive effect on people with neurodegenerative diseases

    .
    Findings published over the past few years have shown that niacin regulates the activity of microglia, important immune cells in the brain, in mouse models of Parkinson's disease, glioblastoma and multiple sclerosis.
    in

    .
    Preliminary evidence for this protective effect has now been shown in a mouse model of Alzheimer's disease

    .

    Clinical trials of niacin for other neurodegenerative diseases have begun, and at least one drug for Alzheimer's is awaiting approval
    .

    Niacin and Alzheimer's disease -- here's an initial link between the two

    Niacin is an essential nutrient obtained from food and supplemental sources such as fish, beef, chicken, and whole grains
    .
    While vitamin intake was not associated with a reduced risk of death, heart attack, or stroke, its pharmacological effect was to increase high-density lipoprotein (HDL) cholesterol

    .

    A lack of niacin can lead to pellagra, a condition that can lead to dementia (among other consequences)
    .
    Since the 1980s, researchers have been exploring whether dietary niacin could help stave off certain neurodegenerative diseases

    .
    For example, a study in a group of older adults in Chicago from 1993 to 2002 calculated niacin intake from dietary data on the participants' food and supplement consumption

    .
    The team found that simultaneous intake from both sources was inversely associated with the development of Alzheimer's disease, and intake from food sources was also inversely associated with cognitive decline

    .
    A study published in 2017 also found a beneficial relationship between dietary niacin intake during adolescence and better cognitive function later in life

    .

    The findings may not be "especially convincing," said Gary Landreth, an Alzheimer's disease researcher at Indiana University School of Medicine
    .
    But he said the existence of such a potential link was "provocative"

    .
    When Miguel motiinho joined Landreth's lab in 2016, the pair decided to ask about the link to see if it existed outside of epidemiological observation

    .

    In addition to the epidemiological link between niacin, cognitive function and Alzheimer's disease, there was another piece of evidence that caught motiinho's attention
    .
    He said he was intrigued by how the so-called ketogenic diet could be linked to the treatment or prevention of Alzheimer's and other neurodegenerative diseases

    .
    One thing the diet does, he adds, is it increases the production of ketone bodies -- molecules produced by the liver from fatty acids during caloric restriction -- that interact with the g-protein-coupled receptor HCAR2 (also known as HCAR2).
    GPR109A), niacin has a high affinity for HCAR2

    .

    Based on both pieces of evidence, Motiinho said, he began to wonder where the niacin receptors are expressed in the brain
    .
    Together with Landris and colleagues, he first explored this question in a mouse model of amyloid pathology -- the accumulation of amyloid-beta plaques, a hallmark of Alzheimer's disease

    .
    They found that Hcar2, the gene encoding Hcar2, was significantly more expressed in the hippocampus and cortex of the affected mice compared to control mice

    .
    When studying postmortem brain tissue in humans, the authors also found that the receptor was more highly expressed in samples from Alzheimer's patients compared to those who had not been diagnosed with dementia

    .

    The expression of this receptor was specifically associated with microglia: when these immune cells were depleted, Hcar2 mRNA levels dropped significantly, while when microglia repopulated, expression recovered
    .
    Furthermore, Hcar2 expression was increased in microglia surrounding amyloid beta plaques compared with microglia not involved in amyloid beta plaques

    .
    The activity of this gene appears to play a beneficial role in how microglia interact with amyloid plaques—mice lacking Hcar2 showed higher plaque burdens in their brain tissue and increased neural yuan loss

    .

    These results answer Moutinho and colleagues' question: In the brain, HCAR2 receptors are mainly expressed in microglia, and more specifically, in those individuals with Alzheimer's disease
    .

    Niacin may stimulate protective microglial activity

    Microglia are macrophages that inhabit the brain
    .
    They are constantly monitoring the environment, ready to protect neurons from microbial or parasitic infection

    .
    However, these immune cells do not appear to be specifically programmed to target amyloid plaques in Alzheimer's disease

    .
    "Microglia have never been beneficial or harmful to Alzheimer's during evolution," said David Morgan, a Michigan State University neuroscientist who was not involved in the niacin study.
    guidance

    .

    As a result, microglia may have "very complex responses" to "signals" from amyloid aggregation and other disease hallmarks, he said -- many of these responses may help protect against parasitic infections, but are not seen in neurodegeneration In the context of disease, some may be beneficial while others may be detrimental
    .
    In fact, studies have shown that the phagocytic activity of microglia against amyloid-beta aggregates can be protective, but if these cells are overactive, they secrete inflammatory factors that damage neurons and worsen Alzheimer's pathogenesis of the disease

    .

    Because motiinho and his colleagues found that microglial protective activity is stimulated by the HCAR2 receptor, to which niacin is bound, they tested whether daily doses of the FDA-approved, oral formulation of niacin, Niaspan, for 30 days could modify the disease development of mouse models
    .
    The team reported that mice treated with Niaspan showed improved working memory, reduced plaque formation and reduced neuronal loss compared to controls

    .

    As expected, Niaspan did not achieve this improvement in mice lacking the HCAR2 receptor
    .
    In the brain, HCAR2 is present almost exclusively in the microglia cells of animals with Alzheimer's, making it "almost like a natural target" because only these cells are sensitive to the treatment, Moudinho said

    .

    While Morgan acknowledges that the authors "have fairly compelling data that they did activate microglia with Niaspan therapy and did slow the phenotype," he noted that they didn't actually treat Alzheimer's, but "Amyloid deposits," which are not the only feature of the disease
    .
    He added that the reason he raised the question was that his team had done something with microglia that "favored amyloid pathology, but (worsened) tau pathology" -- another feature of the disease, Associated with deleterious aggregation of different proteins

    .

    Nonetheless, the authors also quantified the expression of Alzheimer's-related genes in treated and untreated mice, Morgan said, and the activation pattern they report is "one of the kinds of activation you'd expect to see that may have an effect on Alzheimer's disease.
    " useful drugs"

    .
    For example, he noted that in patients treated with Niaspan, "they didn't see an increase in what we call a pro-inflammatory protein," which is thought to be involved in tau pathology

    .
    However, when planning to treat Alzheimer's patients, "you need to be very confident .
    .
    .
    you're not clearing the amyloid, you're exacerbating the pathological changes in tau," he added

    .
    Morgan noted that further research should assess Niaspan's effect on tau -- something the authors acknowledge in their paper

    .

    Prospects for clinical application of niacin in Alzheimer's disease and other neurodegenerative diseases

    Wee Yong, a neuroimmunologist at the University of Calgary who was not involved in the study but was peer-reviewed, said it was "very important work" because of "the field of Alzheimer's research.
    " It's been a while," trying to find a way to eliminate amyloid-beta plaques

    .
    Niasban's effect on Alzheimer's "certainly needs to be tested in humans, but this is .
    .
    .
    ripe for clinical translation," he said

    .

    This is the first time a link between niacin and Alzheimer's disease has been demonstrated in laboratory experiments
    .
    Recent studies by other groups, including Yong, have reported similar effects of niacin on other neurological disorders

    .
    In 2020, Yong and colleagues demonstrated that niacin enhances the phagocytic activity of microglia, specifically its ability to clear myelin debris in cultured cells and in a mouse model of multiple sclerosis

    .
    "Treatment with niacin rejuvenates .
    .
    .
    microglia remove myelin debris, which improves myelin repair," Yong said

    .
    This protective effect is also mediated by the HCAR2 receptor

    .

    Yong said his team discovered niacin by screening more than 1,000 generic drugs while looking for a drug that could stimulate myelin repair
    .
    According to Yong, he and his colleagues are trying to launch a clinical trial to test niacin for multiple sclerosis, but first they "need to have more confidence in the lab results

    .
    "

    Yong and his collaborators also reported that mice affected by glioblastoma, a cancer that occurs in the central nervous system, had slower tumor growth and longer survival when treated with niacin
    .
    The compound stimulates microglia and other immune cells to engulf and kill tumor cells

    .
    Based on these findings, a clinical trial of niacin for the treatment of glioblastoma is currently underway at the University of Calgary

    .

    Research into Parkinson's disease has also revealed a potential role for niacin
    .
    Treatment with this vitamin has been shown to reduce neuroinflammation in these patients, and analysis of their blood samples showed that HCAR2 is also a mediator of this mechanism

    .
    Researchers at Augusta University in Georgia have found that niacin can even stimulate macrophages (a type of immune cell that often work in conjunction with microglia) to switch from pro-inflammatory cells to Anti-inflammatory cells

    .
    The team is currently conducting a clinical trial to test the effects of niacin on this neurodegenerative disease

    .

    Niacin has not been tested in humans for Alzheimer's disease
    .
    Jean Harry, a neurotoxicologist at the National Institute for Occupational Safety and Health in Durham, North Carolina, said that although the formula used by Moudinho and his colleagues was niacin that was For a drug approved for consumption, "it's not easy to get enough substances into the brain parenchyma from some kind of systemic dose, even those that can cross the blood-brain barrier

    .
    " So, she adds, when applying it In humans, researchers need to consider the possible side effects of the dose levels niacin enters the brain, and how this will affect peripheral macrophages

    .

    Landreth Grant said his team recently submitted a proposal for a two-year pilot clinical trial aimed at evaluating whether niacin supplementation causes Alzheimer's disease and biomarker changes "to validate our niacin into the brain at physiologically relevant levels
    .
    " He added that side effects currently associated with niacin treatment, such as skin flushing, are "easy to address.

    "

    "We're very excited about this," Landers concluded
    .

    Niacinamide: Niacin's sister molecule has also been proposed for Alzheimer's

    Niacinamide, also known as niacinamide, is another form of vitamin
    B.
    Although nicotinic acid and nicotinamide have different molecular structures, both play important roles in the biosynthesis of NAD and its reduced form, NADH.
    The NADH molecule is involved in the synthesis of ATP, which cells use as a readily available energy source

    .

    Niacinamide has also been implicated in central nervous system protection, although the mechanism is different from that described for niacin
    .
    For example, in a mouse model of Alzheimer's disease, nicotinamide treatment reduces neuronal susceptibility to amyloid-beta toxicity and improves cognitive performance primarily by enhancing brain bioenergetics

    .
    This form of vitamin B also reportedly reduces a tau protein in a mouse model of Alzheimer's

    .
    Research linking nicotinamide to beneficial outcomes has driven a number of ongoing clinical trials, mostly in the United States

    .

    In an email, Indiana University School of Medicine researcher Miguel moutinho explained that in the context of Alzheimer's disease, "in the brain.
    .
    .
    HCAR2 activation is one of the primary mechanisms of niacin's action

    .
    The amide may be more involved in the production of NAD

    .
    "

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