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Polyphenols in the Protection Against Cardiovascular Disease and Dementia
In a recently published study—NutriNet-Santé (10/2018)—that included the analysis of dietary records of 84,158 French adults that spanned between May 2009 and June 20017— the study authors concluded found that “Higher intakes of polyphenols, especially anthocyanins...
Alzheimer’s Prevention Trials—The Future Looks Promising
Current prevalence estimates (2016) for late-onset Alzheimer’s disease LOAD in the United States (U.S.) is approximately 5.1 million.(1) By 2050 the projected prevalence of LOAD is expected to escalate to 13.8 million and a staggering 106.8 million worldwide.(2,3)
Inflammation and Alzheimer’s Disease—Cause, or Effect?
The role of chronic inflammation in degenerative diseases associated with aging is considered to be a primary vector for the progression of neurodegenerative disorders and a powerful factor that underlies their etiology. One needs only to look at the leading causes of...
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MEMBER ACCESS: PFAS—The Little-Known Forever Chemicals are Emerging as Dangerous Neurotoxicants
A host of environmental toxins pose a significant health risk to the integrity of your brain (neurotoxins). Neurotoxins are ubiquitous and your exposures to many of them may be passing under your radar. This is especially true of a family ...
MEMBER ACCESS: Mercury Depletes Glutathione Peroxidase-Toxic Mechanisms In Alzheimer’s Disease Risk
The research demonstrating the deleterious and toxic effects of mercury on brain function and structure in neurodegenerative disease processes is plentiful. Adding to the research literature, a May/2009 study demonstrated that methylmercury* induces neurotoxicity, by significantly inactivating one the brain's ...
MEMBER ACCESS: Oxidative Stress and the Thromboxane Receptor—A Central Pivot in the Production of Neurofibrillary Tangles
New research published Oct. 13 (2014) by the journal Neurobiology of Aging revealed that the free radicals* produced during oxidative stress in Alzheimer's disease (AD) bind to a protein receptor in the brain designated as the: Thromboxane Receptor A2 (TP) ...
MEMBER ACCESS: TREM2 genetic variants in Alzheimer’s disease
Two recently published studies (2013) on a rare variant of the TREM2 gene (triggering receptor expressed on myeloid cells 2), designated as R47H, was shown to increase the risk of developing Alzheimer’s disease. Individuals with the variant may be up ...
MEMBER ACCESS: Blueberry Polyphenols Protect the Brain from the Degenerative Processes Associated with Brain Aging and Alzheimer’s Disease
The study of plant and fruit polyphenols, a rich source of dietary antioxidants, represents one of the most promising areas of research in the field of anti-aging, and the prevention of degenerative disorders such as Alzheimer's disease. Recent and ongoing ...
MEMBER ACCESS: Brain-Derived Neurotrophic Factor—Growth Factors in Neurogenesis and the Protection Against Alzheimer’s Disease Progression
By Ralph Sanchez, MTCM, CNS, D.Hom. One of the longest held thoughts about damage to our brain's cells (neurons) was that once they're lost, it was a fait accompli. Diseased and dying neurons were once considered damaged goods, never to ...
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#type3diabetes #gutinflammation #alzheimersrisk![]()
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While the headline to an article linked to below suggests that the "liver is key" in the link between type 2 diabetes and late-onset Alzheimer's disease, (LOAD) it sorely misses the mark on the main driver of that association—cardiometabolic disease—which has been described in numerous studies for the past two-plus decades (The Diabetic Brain in Alzheimer's Disease).![]()
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What the article does point out accurately is the role of gut inflammation that underlies a key pathway in the gut-brain axis and the risk for LOAD.![]()
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A recent study highlighted in the article report describes the role of JAK3 in the upregulation of proinflammatory cascades that include the liver.![]()
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Yes, there is several key inflammation mediated linkages between the gut and liver and one includes JAK3—a key protein/enzyme that is IMPORTANT in maintaining immune system development and function, and gut mucosal barrier structure and function.![]()
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However, an unhealthy diet and an unbalanced gut microbiota (dysbiosis) are primary proinflammatory triggers that leads to an aberrant JAK3 signaling pathway that is a component of proinflammatory pathways that may include liver inflammation responses which feed forward microglial-mediated neuroinflammatory cascades. (Microglia are the immune cells of the central nervous system)![]()
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Dr. Kumar, the lead author of the study titled "Mechanistic Role of Jak3 in Obesity-Associated Cognitive Impairments" did show in her study that a high-fat diet in mice—a typical model for diet induced inflammation and cardiometabolic disease—was a mediator of neuroinflammtory responses triggered by JAK 3 that "lead to compromised microglial-functions-mediated increased deposition of β-amyloid (Aβ) and hyperphosphorylated Tau (pTau), which are responsible for cognitive impairments."![]()
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All in all, yet another study that builds on the shared pathophysiological pathways that links diet, cardiometabolic disease, gut dysbiosis and gut inflammation in the risk for LOAD.![]()
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Think ahead and institute a LOAD biomarker-guided prevention focus that includes cardiometabolic and gut health biomarkers.![]()
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And, for a more complete overview of the gut-liver-brain axis in the risk for LOAD, please listen in to my podcast episode titled "Modifiers of the Gut-Brain Axis in the Risk for Dementia and Alzheimer’s Disease"![]()
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@ podcasts.apple.com/us/podcast/brain-detoxification-part-2-the-gut-liver-brain-axis/id1614865183?![]()
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www.asbmb.org/asbmb-today/science/032324/how-might-diabetes-lead-to-alzheimers
How might diabetes lead to Alzheimer’s? Study suggests liver is key
www.asbmb.org
Researchers trace a path from the gut to the brain and say managing diabetes could help to prevent dementia
#freewaterMRIs #alzheimersbiomarkers #vasculardementia![]()
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In the news ... another not so new MRI assessment methodology—"free-water" imaging—that serves as a biomarker evaluation in the risk for vascular dementia, Parkinson's and Alzheimer's disease.![]()
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The report linked to here from the University of San Francisco (USF) describes the use of free-water imaging (diffusion MRI) as a potential tool in the diagnosis Alzheimer's disease in the asymptomatic (no clinical symptoms) or the pre-clinical stage of the disease process.![]()
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What is novel about the study findings detailed in the USF article is the ability of diffusion MRI to detect brain abnormalities and damage that is beyond the scope of what a PET imaging assessment is able to provide.![]()
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For example, PET exam can detect amyloid and tau protein burdens early in the continuum of the Alzheimer's disease process.![]()
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However, this study demonstrated that negative PET scans were in direct conflict with the positive finding of beta=amyloid blood tests (beta-amyloid 42/40 ratio), in the study participants.![]()
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The study authors stated that such brain changes were noticeable "in 66 total regions, as compared to those with a negative amyloid blood test and a negative amyloid PET scan,."![]()
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Furthermore, “Our findings suggest there seem to be events occurring both in the blood and in the brain before you detect amyloid positivity in the brain.” The latter point is in reference to the use of PET scans.![]()
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Additionally, increased brain free-water correlated to accelerated neuroinflammatory cascades and brain shrinkage (atrophy).![]()
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Not included in report is the use free-water imaging in detecting "white matter hyperintensities" (WMHs), which is a significant risk factor associated with strokes, and the increased risk for vascular impairment, vascular dementia and late-onset Alzheimer's disease.![]()
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Free water imaging appears to be a superior risk assessment over currently available and traditional MRI scans in differentiating the cognitive decline associated with VD from LOAD—with or without the presence of WMHs.![]()
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Last year I reported on the Quest announcement (8/23) and the concerns raised with regard to the direct-to-consumer Quest Diagnostics beta-amyloid blood assessment (AD-Detect™ Test) that the study authors used.![]()
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AD-Detect is designed to evaluate the risk status for Alzheimer's disease (AD) in people that that are exhibiting signs of mild cognitive impairment (MCI) or dementia, BUT it is not a diagnostic evaluation for AD.![]()
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Late-onset Alzheimer's disease (LOAD) is a multifactorial disease process and there are a host of biomarkers that can shed a great deal of light on an individual's risk for LOAD as they age.![]()
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Leveraging a robust set of biomarkers, apart for blood and brain beta-amyloid assessments, can provide significant insights about your risk for LOAD, and in turn empower a prevention minded strategy.![]()
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Indeed, individuals at risk for LOAD can gauge that risk EARLIER in life through a host of genetic, biochemical, neuroimaging, and metabolic biomarkers that can be integrated a comprehensive risk evaluation for cognitive impairment and dementia as they age. ![]()
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ufhealth.org
New research published today suggests there is a link between abnormal blood levels of amyloid — a protein associated with Alzheimer’s disease — and subtle...
#galantamine #badsupplements #alzheimersmedications ![]()
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Not surprised ... yet another study report on adulterated or poor quality supplements sold online.![]()
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Over the past few years I've consistently reported on study outcomes that showed the benefits of various types of supplements and nutraceuticals, in mitigating the risk for cognitive impairment and late-onset Alzheimer's disease.![]()
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Numerous trials and studies have shown that: ![]()
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• protein/amino acids, ![]()
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• fats (omega 3, short chain and medium chain fatty acids), ![]()
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• phytochemicals (phenolics, coumarins, terpenoids and alkaloids), ![]()
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• multivitamin-mineral and antioxidant supplements, ![]()
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• pre and probiotics, ![]()
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• nutraceutical formulations, and![]()
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• medical foods![]()
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as promising and proven interventions for optimizing cognitive health, and in the prevention of the damaging structural and functional brain changes associated with Alzheimer's disease.![]()
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However, with all good intentions in mind, most individuals lack the expertise required for selecting science-based and quality supplements that meet the most stringent quality control and review guidelines.![]()
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Additionally, hype often trumps science which leads to bad choices on bad supplements.![]()
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The report from MEDPAGE TODAY linked to here on galantamine supplements illustrates just how unreliable and risky the process of selecting certain supplements online can be.![]()
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Not only did 9 of 10 galantamine supplements fail to meet the ingredient amount stipulated on the label (as little as 2% of the of the labeled quantity), 30% of the galantamine products were contaminated with bacteria that could produce harmful side effects.![]()
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Galantine is a plant-derived alkaloid from Caucasian snowdrop and several plants (Amaryllidaceae bulbs), and it is an FDA approved prescription medication (RAZADYNE®) for the treatment of mild to moderate Alzheimer dementia.![]()
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Galantamine functions as a acetylcholinesterase inhibitor (AChEI) which enhances the the levels of synaptic acetylcholine—a key molecule and neurotransmitter that supports memory and learning mechanisms.![]()
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Well known cholinesterase inhibitor medications include Aricept (donepezil), Exelon (rivastigmine), and Razadyne (galantamine).![]()
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Despite some reports to the contrary, the Council for Responsible Nutrition emphasizes that galantamine is not a legal OTC dietary supplement.![]()
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NONE of my trusted and reputable supplement manufacturer providers that cater to professionals distribute galantamine.![]()
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However, there a several well-studies and plant-derived AChEI such as Huperzine A that are legally distributed and sold by reliable manufacturers that employ a host of rigorous in-house and independent quality control and safety precautions.![]()
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Choose wisely and seek the guidance of an experienced professional.![]()
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Alzheimer's Supplements Fail Compared With Generic Drugs
www.medpagetoday.com
Prescription galantamine drugs were labeled accurately, but dietary supplements were not
#cognitivereserve #lifestylefactors #alzheimersrisk![]()
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Older age and the aging process is frequently cited as the primary risk factor associated with late-onset Alzheimer's disease (LOAD) and dementia.![]()
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As stated on the article forward here re the role of lifestyle in preserving cognitive function into a ripe old age, the authors state " ... as individuals age, there is a progressive accumulation of dementia-related brain pathologies such as beta-amyloid, which raises the question of whether the lifestyle is associated with cognition independently of dementia-related brain pathologies."![]()
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The question has been explored in numerous studies that have investigated the role of diet, nutrition, and lifestyle factors in staving off LOAD and dementia in later life.![]()
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And in fact, If one's brain IS under the assault of the the neurodegenerative disease process associated with LOAD as you get older, diet, nutrition, and lifestyle factors (e.g., exercise) are essential for safeguarding your brain from shrinkage and the withering of your cognitive faculties as time wears on.![]()
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Additionally, education, having a brain challenging job, and regularly engaging in social and other activities that challenge the brain can contribute to a more resilient brain.![]()
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How so?![]()
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Since the 90s, post mortem examinations and population studies have shown that diet and environmental factors are critical elements in building a brain and cognitive reserve throughout life.![]()
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What does such a "reserve" represent?![]()
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A cognitive reserve can be defined as a functional reserve of neurons and synapses that are integrated into alternate neural networks. ![]()
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Similarly, a brain reserve is a structural reserve—a build up of neurons or synapses that are unaffected by pathology. ![]()
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Thus, structure enables function and supports a brain resilience that protects against the neuropathological hallmarks (beta-amyloid and tau protein aggregations) and degenerative disease process linked to LOAD.![]()
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Indeed, such a brain and cognitive reserve is vital in buffering against the loss of structure (brain shrinkage), and preserving the the functional capacity to recruit higher level (executive function) cognitive processing as we age.![]()
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It is the stuff of super-agers—"people in their 80s who have the memory function of people 30 years younger"![]()
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It is never too late to initiate the practices and daily activities that nourish brain resilience, but the sooner the better.![]()
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Think ahead!![]()
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Even With Alzheimer's Pathology, Healthy Lifestyles May Preserve Cognition
www.medpagetoday.com
More data support the idea of 'cognitive reserve'THE ALZHEIMER'S SOLUTION
TestimonialsWhat a tremendous resource! Thank you for putting all of this great research in one place! I am also extremely interested in warding off a family history of Alzheimer’s and Dementia. Medicine can be so very powerful when we are able to identify the biochemical inefficiencies, apply specific dietary and nutritional remedies and compile a protocol to heal not just an individual, but generations. Thank you Ralph!
This is an incredible article! Very powerful information! Thank you so much for putting it together the way that you have. This information needs to get out to the masses. You explained that very well.
Absolutely the BEST article I have read on the insulin/AD connection. As always, your brilliance is very much appreciated!
Thank you so much for this well written article. Looking forward to future updates. Thanks for this well illustrated, researched, and detailed yet succinct article.