Niacinamide Alzheimer’s Clinical Trial

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.

The Kronos Early Estrogen Prevention Study

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To assess effects of menopausal hormone therapy and normal aging on cognitive performance and imaging markers of brain structure in women approximately thirteen years after enrolling in the KEEPS trial. KEEPS participants were randomized to oral or transdermal estrogen treatments or placebo within three years of menopause. This is a follow up study of these women approximately thirteen years after randomization No treatments are given as part of this study any current hormonal treatments are by choice and prescribed by the participant’s personal physician.

at UCSF

Niacin Intake And Cognitive Change In The Entire Study Population

We also examined whether dietary intake of niacin was associated with 6 year cognitive change among 3718 people in the larger study population. Although this type of analysis is not specific to AD, it provides an objective and sensitive measure of gradual decline, the central characteristic of this disease. Much of the cognitive decline in the population is probably due to disease processes associated with AD, which is the leading cause of dementia, followed by vascular dementia.

The mean cognitive score at the initial assessment was 0.18 , and the average annual decline was 0.042 standardised units per year. Food intake of niacin had a linear protective association in both continuous and categorical models. In the continuous model adjusted for demographic confounders, the rate of cognitive decline decreased by 0.019 SU/year per ln increase in intake . The effect was attenuated slightly after additional control for dietary intakes of antioxidant nutrients and folate, multivitamin use, smoking and alcohol use, stroke, heart disease, diabetes, and hypertension. Substitution of each of the other B vitamins for folate produced similar results.

Table 3

Adjusted effects of niacin intake from food ) on the rate of cognitive change over 6 years, among the total cohort of 3718 participants, and among 2824 participants with no history of stroke or myocardial infarction at baseline or first follow up, Chicago Health and Aging Project, 19932002

Figure 1

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See Microglia As Therapeutic Targets In Neurodegenerative Diseases

Based on the new data of niacin limiting Alzheimers progression in mice and the fact that it is FDA approved, I believe it is worth a clinical trial in individuals with mild cognitive impairment and early Alzheimers disease, University of Florida neuroscientist Malú Tansey, who is not involved in any of these niacin studies, writes in an email to The Scientist. Currently, clinical trials testing niacin for other neurodegenerative diseases are already underway, and at least one for Alzheimers treatment is awaiting grant approval.

Nicotinamide Does Not Affect A Pathology

We previously showed that soluble A and soluble tau, which both accumulate within the somatodendritic compartment of neurons, can underlie the cognitive deficits in the 3xTg-AD mice . Hence, we sought to determine whether the improved cognitive performance could be attributed to an effect of nicotinamide on A pathology. ELISA analysis of A levels in both the detergent-soluble and -insoluble fractions from brain homogenates of control and nicotinamide-treated 3xTg-AD mice revealed no statistically significant differences between groups . Consistent with the ELISA findings, immunohistochemical staining for A-like immunoreactivity did not reveal any discernable differences in intraneuronal A accumulation in cell bodies of the hippocampus, amygdala, and cortex between the two groups . Steady-state levels of APP were also unchanged compared with controls, as were levels of A*56, an A oligomer linked to cognitive decline , and the C-terminal fragments of APP C83 and C99 . These results show that A production is not altered by nicotinamide, and that the beneficial effects of nicotinamide on cognition must occur through another mechanism.

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An Electronic Clinical Decision Support Tool To Reduce Low

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The goal of this study will be to design, implement and test the impact of a quality improvement intervention that uses an EHR CDS tool among physicians newly ordering an antipsychotic medication for older adults with ADRD. The study team hypothesizes that the intervention will reduce each participating clinician’s pill days per patient prescribed.

at UCLA

Nia Statement On Report Of Lecanemab Reducing Cognitive Decline In Alzheimers Clinical Trial

Pharmaceutical companies Eisai and Biogen recently announced data for a phase 3 Alzheimers disease clinical trial. The results show that lecanemab, an anti-amyloid antibody, slowed the rate of cognitive decline by 27% in an 18-month study involving participants experiencing the early stage of Alzheimers. The incidence of adverse events was 21.3% for those who received lecanemab and 9.3% for those who received a placebo. About 25% of the U.S. participants in this study were Hispanic and African American.

The NIH National Institute on Aging eagerly awaits publication of the data in a peer-reviewed scientific journal. Potentially promising outcomes such as this one are the result of sustained public investment in medical research, the tireless work of scientists around world, and the help of people living with Alzheimers and their caregivers. Although NIA did not fund the lecanemab study, our decades of research paved the way for this Alzheimers trial that notably met its primary and secondary endpoints.

NIA-funded scientists will also continue to identify and test new dementia drug candidates, advance comprehensive models of care, develop new biomarker tests, explore disease risk and possible protective factors throughout the life course, examine disparities in dementia prevalence and care, and improve the understanding of the role of genetics and other disease mechanisms.

Richard J. Hodes, M.D., Director, National Institute on Aging, National Institutes of Health

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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.

Salsalate In Patients Mild To Moderate Alzheimer’s Disease

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The purpose of the study is to test the safety and tolerability of twice daily Salsalate in patients with mild to moderate Alzheimer’s Disease. Half of the participants will receive Salsalate and half will receive placebo during the 1-year duration of the study.

at UCSDUCSF

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Niacin Prevented Cognitive Decline In Mice

In an earlier study researchers found that nicotinamide or niacin was able to prevent cognitive decline in mice.

Results of these studies strongly suggest that niacin might be useful in a therapeutic way for treating Alzheimers patients. More studies will need to be done with human clinical trials to see if these effects on mice can also apply to people suffering from dementia and Alzheimers.

If studies with humans also show that niacin can protect the brains of people suffering from Alzheimers, research will be necessary to show at what dosages treatment with niacin is effective and safe.

Dominantly Inherited Alzheimer Network Trial: An Opportunity To Prevent Dementia A Study Of Potential Disease Modifying Treatments In Individuals At Risk For Or With A Type Of Early Onset Alzheimer’s Disease Caused By A Genetic Mutation Master Protocol Dian

open to eligible people ages 18-80

The purpose of this study is to assess the safety, tolerability, biomarker and cognitive efficacy of investigational products in subjects who are known to have an Alzheimer’s disease-causing mutation by determining if treatment with the study drug slows the rate of progression of cognitive impairment and improves disease-related biomarkers.

at UCSD

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Mri And Pet Biomarkers For Cognitive Decline In Older Adults

open to eligible people ages 60-85

The purpose of this research study is to understand the factors that underlie changes in thinking and memory with increasing age. The investigators will test the usefulness of MRI, PET, and cognitive testing in detecting subtle changes in the brain that precede cognitive decline. An addendum to this study includes additional PET scans to examine the relationship between tau protein in the brain and cognitive decline. Tau is a protein that is known to form tangles in the areas of the brain important for memory, and these tau tangles are a hallmark of Alzheimer’s disease. This sub-study research aims to look at the tau accumulation in the brain using an investigational drug called MK-6240, which is a radio tracer that gets injected prior to a positron emission tomography scan.

at UC Irvine

Benefits Of Boosting Nad+ Metabolism In Animal Models

Stimulating NAD+ metabolism with NMN or nicotinamide riboside extends healthspan and mitigates premature ageing diseases in mice. Long-term oral administration of NMN suppresses age-associated weight gain, enhances energy metabolism, improves insulin sensitivity and prevents age-linked changes in gene expression. Following treatment, the metabolism and energy levels of older mice resemble those of younger mice.

Evandro Fei Fang, a molecular gerontologist leading an anti-ageing laboratory at the University of Oslo, Norway, has been examining the effects of treatments that increase intracellular NAD+ on animal models of accelerated ageing diseases such as ataxia-telangiectasia and Werner syndrome, and neurodegenerative diseases, including Alzheimers disease. NAD+ participates in a broad range of cellular pathways linked to neuronal survival and function, Fang says. With Vilhelm Bohr at the National Institute on Ageing, Baltimore, United States, Fangs team has shown that by stimulating neuronal DNA repair and selectively degrading damaged mitochondria via mitophagy, NMN can protect neurons against pathological aggregated proteins, such as p-tau, and improve memory in animal models of Alzheimers disease as well as improve healthspan and lifespan of animal models exhibiting accelerated ageing diseases. These results could indicate the importance of maintaining mitochondrial quality for healthy ageing and NMN as a strategy to prevent mitochondrial dysfunction.

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Care Ecosystem: Navigating Patients And Families Through Stages Of Care Extension Trial

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This is an extension trial of a prior trial . Both persons with dementia and their caregivers were enrolled as dyads. The purpose of this randomized clinical trial is to evaluate the benefits of a program that supports model care for PWD and their caregivers. Whereas the prior trial only delivered care and examined outcomes up to 12-months, this trial extends care and outcome measurement for 5 years or until death, and includes all dyads where the caregiver reported high caregiver burden at pre-randomization baseline for the original trial. Participants were recruited from California, Nebraska and Iowa. Participants determined to be eligible were consented and randomized into one of two groups. Two thirds of dyads were enrolled into Navigated Care that provided them with phone-based assistance in meeting important benchmarks in their care, for example completion of legal and financial planning and strategies for minimizing caregiver burden. One third of dyads were enrolled to a control group, entitled Survey of Care. Outcomes were unchanged from the original trial except for the addition of time to long term care placement and are detailed below.

at UCSF

Why Is Diversity Important In Clinical Trials

Researchers need participants who represent all types of races and ethnicities, genders, geographic locations, and sexual orientations.

When research involves a group of people who are similar, the findings may not apply to or benefit everyone. When clinical trials include diverse participants, the study results may have a much wider applicability.

Having diverse people in studies can help researchers understand how dementia affects certain groups, why some communities are disproportionately affected by certain dementias, and which treatments or prevention strategies may be most effective in particular groups.

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Treatment Of Alzheimer’s Disease With Stabilized Oral Nicotinamide Adenine Dinucleotide: A Randomized Double

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• Psychology, Medicine
• Drugs under experimental and clinical research

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• Frontiers in Cell and Developmental Biology

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Niacin And Alzheimer Dementia

The news media recently reported that huge doses of an ordinary vitamin appeared to eliminate memory problems in mice with the rodent equivalent of Alzheimers disease. They then quickly added that scientists arent ready to recommend that people try the vitamin on their own outside of normal doses.

In other words, extra-large amounts of a vitamin are helpful, so dont you take them!

That does not even pass the straight-faced test. So whats the story?

Researchers at the University of California at Irvine gave the human dose equivalent of 2,000 to 3,000 mg of vitamin B3 to mice with Alzheimers. It worked. Kim Green, one of the researchers, is quoted as saying, Cognitively, they were cured. They performed as if theyd never developed the disease.

Specifically, the study employed large amounts of nicotinamide, the vitamin B3 widely found in foods such as meat, poultry, fish, nuts and seeds. Nicotinamide is also the form of niacin found, in far greater quantity, in dietary supplements. It is more commonly known as niacinamide. It is inexpensive and its safety is long established. The most common side effect of niacinamide in very high doses is nausea. This can be eliminated by taking less, by using regular niacin instead, which may cause a warm flush, or choosing inositol hexaniacinate, which does not. They are all vitamin B3.

The Irish Times reiterated it:

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See Replacing Microglia Treats Neurodegenerative Disease In Mice

Because Moutinho and colleagues found that microglial protective activities are stimulated by the HCAR2 receptor, and as niacin is known to bind to it, they tested whether a daily dose of the FDA-approved oral formulation of niacin, Niaspan, for 30 days could alter the development of the disease in their mouse model. The team reports that mice undergoing this treatment showed improved working memory, reduced plaque formation, and diminished neuronal loss, compared to those treated with a control solution without Niaspan.

As expected, Niaspan did not achieve this improvement in mice lacking the HCAR2 receptor. In the brain, HCAR2 is almost exclusively found in the microglia of animals with Alzheimers, making it almost like a natural targeting as only those cells will be sensitive to the therapy, says Moutinho.

While Morgan acknowledges that the authors have pretty convincing data that they are really slowing the phenotype by the activation of microglia achieved with the Niaspan treatment, he notes that they are not really treating Alzheimers, but rather amyloid deposition, which is not the only feature of the disease. The reason he brings this up, he adds, is that there are some manipulations of the microglia his team has performed that benefit amyloid pathology but tau pathologyanother feature of the disease related to the harmful aggregation of different proteins.

Nicotinamide Selectively Reduces Thr231 Phosphorylated Tau

Given that nicotinamide improved cognition in both hippocampal- and amygdala-dependent tasks, but had no effect on A levels, we next investigated its effects on tau pathology. Steady-state levels of human tau were significantly reduced by 20% in nicotinamide-treated mice compared with controls . At 8 months of age, 3xTg-AD mice contain modified tau that is phosphorylated at a number of serine and threonine sites. Steady-state analysis of these phosphotau epitopes revealed no differences in tau phosphorylated at Thr212/Ser214 , Ser199/202 , or Thr181 between the nicotinamide- and vehicle-treated mice. Notably, immunoreactivity against Thr231-phosphotau was markedly reduced by > 60% in the nicotinamide group compared with vehicle . Analysis of insoluble tau levels via filter retardation assay revealed no differences in total human tau, but a trend toward reduction in Thr231-phosphotau that did not reach statistical significance .

In vehicle-treated 3xTg-AD mice, immunostaining for human tau revealed extensive somatodendritic accumulation in neurons of the hippocampus and amygdala, whereas it was absent in cortex . Notably, behavior on novel object recognition, a cortex-dependent task, was not improved with nicotinamide treatment , which is consistent with the lack of tau pathology in cortical brain regions at this age.

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Nicotinamide A Poly Polymerase 1 Inhibitor As An Adjunctive Therapy For The Treatment Of Alzheimers Disease

• 1Centro de Investigación Clínica Avanzada, Facultad de Medicina and Hospital Clínico Universidad de Chile, Santiago, Chile
• 2Sección de Geriatría Hospital Clínico Universidad de Chile, Santiago, Chile
• 3Departamento de Neurociencia, Facultad de Medicina, Universidad de Chile, Santiago, Chile
• 4Biomedical Neuroscience Institute, Facultad of Medicina, Universidad de Chile, Santiago, Chile
• 5Institute for Research in Dental Sciences, Facultad de Odontología, Universidad de Chile, Santiago, Chile
• 6Center for Integrative Biology, Facultad de Ciencias, Universidad Mayor, Santiago, Chile
• 7Departamento de Neurologiìa y Neurocirugiìa, Hospital Cliìnico Universidad de Chile, Santiago, Chile
• 8Departamento de Neurología y Psiquiatría, Clínica Alemana de Santiago, Santiago, Chile

Nicotinamide As An Early Alzheimer’s Disease Treatment

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The purpose of this research study is to test whether nicotinamide, also known as vitamin B3 or niacinamide, taken in high doses, can reduce phosphorylation of tau in people with Mild Cognitive Impairment or mild Alzheimer’s disease dementia.

at UC IrvineUCLA

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