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How COVID-19 might increase risk of memory loss and cognitive decline

by Ralph Sanchez | Oct 20, 2020

By Natalie C. Tronson, Associate Professor of Psychology, University of Michigan Edited by Ralph Sanchez Of all frightening ways that the SARS-COV-2 virus affects the body, one of the more insidious is the effect of COVID-19 on the brain. It is now clear that many...

Lose The Belly Fat And Save Your Brain From Shrinking

by Ralph Sanchez | Apr 18, 2020

The role of obesity in late-onset Alzheimer’s disease is linked to insulin resistance, type 2 diabetes, cardiovascular disease, and chronic inflammation pathways. Not surprisingly, the same cardiometabolic disease patterns are correlated to brain and hippocampal volumes (brain shrinkage).

Late-Onset Alzheimer’s Disease—The Hidden Midlife Crisis

by Ralph Sanchez | Aug 31, 2019

Midlife may be a critical juncture in one's life and a time for contemplating what the rest of it will look like. It may be a time of reflection on time well spent or sheer regret for not having done enough of what you really love to do. Midlife may also be a turning...

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Think Ahead for a Better Brain Tomorrow!

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 ...

Image courtesy of the National Institute on Aging/National Institutes of Health

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 ...

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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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The Alzheimer's Solution

1 month ago

#kynurenine #glucosehypometabolism #alzheimersdiseaseOne of the causative factors in the multiple neurodegenerative cascades associated with Alzheimer's disease (AD) that captured my attention many years ago was the role of mitochondrial dysfunction and impaired energy metabolism that is a central aspect to many chronic health disorders.In the Medical News Today report linked to here, researchers have identified an immunotherapy cancer drug an enzyme that that restores glucose metabolism in the brain via a well known pathway—the kynuerinine pathway."Using an Alzheimer’s mouse model, they found that blocking the enzyme, called indoleamine-2,3-dioxygenase 1, or IDO1, helped preserve memory and cognition in the early stages of the disease."The cancer drug essentially blocked IDO1 which is a component in the kynuerinine pathway, is also a the major route (95%) of tryptophan degradation.Why would blocking IDO1 be potentially important?Increased IDO1 activity is a feature associated with aging, chronic inflammation (inflammaging), and the risk for age-related diseases.Inflammaging and unregulation of the IDO1/kynurenine pathway further exacerbates a proinflammatory terrain of the body and brain which is a significant risk factor for age-related diseases such as cancer, cardiometabolic disease and Alzheimer's disease. Another biomarker in the unregulated IDO1/kynurenine pathway is the Kynurenine/Tryptophan ratio.A skewed Kynurenine/Tryptophan ratio—lower tryptophan and higher kynurenine levels—is an inflammaging biomarker.Excess IDO1 stimulated kynurenine synthesis is associated with:- chronic chronic immune activation and inflammation (inflammaging), - = infections,- stress, sleep disturbances, and - dysregulation of gut microbiota (dysbiosis).Elevated kynurenine also leads to the accumulation of quinolinic acid which is a neurotoxin linked to neuronflammatory responses and neurodegenerative diseases. (Not mentioned in the report)And the increased metabolic shift toward the production of quinolinic acid also results in increased nicotinamide adenine dinucleotide (NAD), which normally is a critical cofactor in energy metabolism and other metabolic/biochemical reactions and pathways.However, the induction of oxidative stress pathways due to elevated quinolinic acid depletes both NAD and ATP levels.All in all, the research report emphasized that kynurenine dysmetabolism in critical housekeeping cells of the brain—astrocytes—and the subsequent shift of the kynurenine pathway is also a factor in the aberrant lactate and glucose metabolism (hypometabolism) seen in people with Alzheimer’s.And not surprisingly, an unregulated IDO1/kynurenine pathway is also associated with brain beta-amyloid and tau protein burdens.However, do we need a cancer drug to blunt IDO1 and restore a normal Kynurenine/Tryptophan ratio and a healthy energy and glucose metabolism in the brain?In my book I detail how glucose hypometabolism in type 3 diabetes is linked to type 2 diabetes and "brain insulin resistance", and the important role astrocytes play in lactate and energy metabolism.The earliest stage (preclinical) in the disease progression of late-onset Alzheimer's Disease (LOAD), is marked by several structural and functional features including inflammaging, and the decline in mitochondrial function and energy metabolism (glucose hypometabolism).Early risk factor assessments by midlife is critical for designing intervention strategies that will prevent the gradual neurodegenerative pathology associated with type 3 diabetes and late-onset Alzheimer's disease.Think Ahead!BrainDefend® ... See MoreSee Less

Alzheimer’s: Novel cancer drug restores cognition, memory loss in mice

www.medicalnewstoday.com

Researchers identified an enzyme that regulates glucose metabolism in the brain and discovered that a cancer drug may help treat early-stage Alzheimer's disease.

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The Alzheimer's Solution

2 months ago

#reelincolbosvariant #earlyonsetAlzheimer'sdisease #dementiadelayThe NPR report linked to here highlights recent research reports on two genetic variants that are linked to the resilience and resistance to Alzheimer's disease in carriers of the PSEN1 gene.The PSEN1 gene is deemed a determinant gene (highly penetrant), and the most common causative factor for early-onset Alzheimer's disease (EOAD).The two protective genetic variants—the ApoE3 Christchurch variant, and the Reelin-COLBOS variants have previously been identified in earlier research findings.Each of those variants are associated with extraordinary delay in cognitive decline and EOAD-related dementia, which normally manifests in carriers of the PSEN1 mutation by their mid-to-late 40s. The ApoE3 Christchurch variant and the Reelin-COLBOS variant carriers, and their respective cases, are participants from the ongoing Columbian kindred study of EOAD, which consists of approximately 6,000 blood relatives, and about 1,200 are carriers of variant—the PSEN1 “Paisa” mutation (Presenilin-1 E280A)—a strong causative factor for EOAD.In the case of the female ApoE3 Christchurch variant carrier, her cognition was intact into her 70s, despite a significant brain burden of tau and beta-amyloid deposition. She eventually exhibited signs of cognitive impairment and Alzheimer's-related dementia at agePlease read more about that remarkable story below in my previous post below this one, and note the description of HSPGs (heparan sulfate proteoglycans)—a key component as to why the ApoE3 Christchurch variant carrier resisted the onset of dementia for so many years.Similarly, the Reelin-COLBOS resilience to dementia tale is about a male carrier of the variant, who also remained dementia-free with a brain riddled with beta-amyloid and tau protein aggregations until the age of 70 when he was diagnosed with cognitive impairment, a dementia two years later.A key region of the Reelin-COLBOS carrier's brain associated with learning and memory—the entorhinal cortex—escaped the heavy tau brain burden associated with EOAD.Reelin protein is a vital and integral component of the extracellular matrix (ECM)—a critical and functional structure which surrounds almost every cell of the body and brain.In the adult brain, reelin exerts several key neuroprotective and neuromodulatory roles that are integral to synaptic plasticity, and learning and memory signaling cascades.For example, reelin has been shown to inhibit the toxic effect of beta-amyloid aggregates on the integrity of synaptic receptor signaling pathways. Note, I describe at length the synaptic disruption of toxic beta-amyloid aggregates on synaptic receptors in my book: "The Diabetic Brain in Alzheimer's Disease".Reelin protein and related ECM mechanisms normally blunts the potential toxicity of beta-amyloid and tau protein processing.With regard to tau protein, Reelin inhibits the spread of tau"seeds" and aberrant formation (hyperphosphorylation) of tau protein tangles (NFTs).Similarly, ECM-related reelin mechanisms are important in blunting beta-amyloid accumulation and toxicity.Reelin also plays a role in the autophagic clearance of beta-amyloid aggregates.All in all, reelin signaling disruption and reelin depletion is linked to the very earliest stages of Alzheimer's disease, is a significant factor in the upregulation of toxic tau and beta-amyloid protein metabolism and deposition, and in the induction of synaptic dysfunction.Finally, the takeaway from those two extraordinary EOAD case studies is that it points to three critical and MODIFIABLE risk factors associated with late-onset Alzheimer's disease.The vital and brain-protective interactions between reelin, HSPGs, and the ECM can be nourished and protected via healthy diet, nutrition and lifestyle habits that blunts neuroinflammatory and oxidative stress cascades that underlies their depletion and dysfunction.Look for my more expanded overview and book on brain resilience and resistance in cognitive super-agers, and how you can get there too.BrainDefend® ... See MoreSee Less

A protein called Reelin keeps popping up in brains that resist aging and Alzheimer’s

www.npr.org

Early in life, the protein Reelin helps assemble the brain. Later on, it appears to protect the organ from Alzheimer’s and other threats to memory and thinking.

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The Alzheimer's Solution

2 months ago

#earlyonsetAlzheimersdisease #apoe3christchurchvariant #dementiapreventionRecently, an uptick on findings derived from the world's largest population study of Columbian Alzheimer's disease kindred that are carriers of a genetic determinant of early-onset Alzheimer's disease (EOAD) have surfaced in traditional and social media reports.The deterministic (autosomal-dominant) EOAD gene, the PSEN1-E280 mutation, is one of several known autosomal-dominant genes (causative) associated with EOAD.Despite the more recent reports, the Colombian autosomal dominant Alzheimer disease (ADAD) longitudinal study began in 1995, and the data analysis report of a retrospective cohort study between 1995 and 2012 which was first published in 2016.Since then, a slew of insightful discoveries regarding the Colombia Alzheimer's disease kindred, have since been published.Case in point, the 2019 case report of a Colombian woman that was found to be a carrier of a rare genetic variant, the rare ApoE3 Christchurch variant (ApoE3ch) that delayed the inevitable onset of dementia associated with EOAD (familial Alzheimer's disease) by approximately, 30 years. She died of cancer at the age of 77 a few years after cognitive impairment and dementia was apparent.In PSEN1 E280A mutation carriers the median age of onset of mild cognitive impairment (MCI) is 45, and onset of dementia is age 49.However, a much more significant finding precedes that 5 year delay report from Mass General.In an effort to unravel the seemingly miraculous and significant 30 year delay in the onset of MCI and dementia in the case of the Colombian female carrier of the PSEN1-E280A mutation and ApoE3ch variant (homozygous), a number of studies since her case report published in 2019 have emerged and shown that the protection imparted by the ApoE3ch variant is linked to a unique characteristic of the extracellular matrix (ECM) and glycosaminoglycans (GAGs) that occur on neurons.So what is the ECM-GAG story all about?The term, glycosaminoglycans (GAGs), are a reference to chains of carbohydrates (polysaccharides, sugar acids), and amino-sugars, and which often sulfated (sulfated GAGs).Sulfated GAGs molecules such as heparan sulfate or chondroitin sulfate, are further linked as side chains to protein anchors (proteoglycans) which along with other molecules (e.g., laminin, fibronectin, hyaluronan) collectively form the extracellular terrain known as the extracellular matrix (ECM).The ECM is a dynamic snd functional structure that is attached to almost every cell of the body and brain, and in the adult brain it serves as a critical structure that mediates signaling cascades which are central to maintaining and optimizing autophagy pathways, and synaptic plasticity.Several studies have shown that the ApoEch variant's ECM-GAG profile (heparan-sulfate proteoglycans) protect against the more severe tau and beta-amyloid protein neuropathology associated with the PSEN1-E280 mutation and EOAD.So what does the remarkable story of the ApoEch variant carrier's case study possibly represent for those of us that are fortunate to not carry RARE genetic mutations linked to familial Alzheimer's disease?Well, a prime takeaway from the rare ApoEch carriers case for most individuals concerned about late-onset Alzheimer's (LOAD) disease and dementia linked to RISK genetic variants such as the ApoE4 variant, is that maintaining and optimizing a healthy ECM-GAG structure is an essential component to pathways connected to autophagy, mitochondrial function, and synaptic plasticity. While the current EOAD research efforts seek to develop drug solutions, LOAD is preventable and the diet, nutrition and lifestyle habits nourish a healthy ECM-GAG structure and environment.Please look for my next post with regard to another genetic variant revelation associated with the Colombian Alzheimer's kindred that sheds yet another insight about an ECM protein (reelin), and how the ECM-reelin synergism is associated with stem cell homeostasis, neurogenesis, and longevity pathways.Note that reelin is also briefly described in the Mass General Brigham article linked to here—https://www.massgeneralbrigham.org/en/about/newsroom/press-releases/one-copy-of-genetic-variant-protects-against-early-onset-alzheimers— which describes the more recent finding linked to the Colombian kindred longitudinal study—a 5 year delay in onset of dementia in heterozygous (one copy) carriers of the ApoE3ch variant.BrainDefend®www.medpagetoday.com/neurology/alzheimersdisease/110724 ... See MoreSee Less

Alzheimer's Onset Delayed by Rare Mutation

www.medpagetoday.com

Just one copy of the Christchurch variant conferred protection

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The Alzheimer's Solution

4 months ago

#cognitivedecline #predictionmodel #alzheimersdementiaIn a study just published, the study authors unveiled the development of an online tool for clinical use that can be used to predict "how fast" cognitive decline would occur "in amyloid-positive patients" with mild cognitive impairment (MCI) or "mild dementia".Amyloid positivity was based on cerebrospinal (CSF) beta-amyloid concentrations (AB42) or amyloid PET.The researchers cited studies that showed the patients with MCI and individuals diagnosed with "mild dementia" due to Alzheimer's disease, were keen on possibly knowing what a realistic future expectation for the progression of the disease might be.The study compiled data from 961 patients with Alzheimer's disease including 310 people with mild cognitive impairment and 651 with "mild dementia."Data biomarkers "incorporated age, sex, cognitive test scores, APOE4 status, amyloid PET or CSF biomarker data, and MRI total brain and hippocampal volume."Adding cardiovascular risk factors to the data did not improve "predictive performance"Additionally, CSF phosphorylated tau biomarkers "aided in the prediction of MMSE decline in our amyloid-positive sample,"The data was used to develop a cognitive decline prediction model based on measurements of Mini-Mental State Examination (MMSE) scores—a widely-used cognitive performance assessment in the evaluation of cognitive function.The MMSE test score range is 0 to 30. A normal score is between 24 and 30.An MMSE score of 0 and 17 is graded as severely impaired, and mildly impaired for scores between 18 and 23.In the study participants, cognitive decline rates increased over time in both groups. In the MCI group, MMSE scores dropped from approximately 26.4 to 25.8 after 18 months, to 24.2 after 3 years, and to 21.0 after 5 years. "In the mild dementia group, mean MMSE scores fell from 22.4 to 19.8, 15.3, and 7.8, respectively."However, in a hypothetical model of intervention prediction based on 12 risk factors cognitive decline was reduced by up to 50% AND the time for conversion from MCI to mild dementia (MMSE of 20) would be 8.6 years which potentially can add invaluable years to an individuals' quality of life experience.Notably, the prediction models can be shown with a "calculator with visualization as a prototype tool to discuss prognosis, the uncertainty surrounding the predictions, and the impact of intervention strategies with patients."While the study researchers stated that "The personalized predictions can give patients a general indication of their Alzheimer's course", there was no commentary about the possible prevention of cognitive decline in the MCI group which is a critical time for possibly reversing the course of the disease.After all, there are preliminary case studies findings that demonstrate that MCI due to vascular disease and Alzheimer's disease can be reversed to normal with personalized lifestyle and nutraceutical interventions utilizing a progressive biomarker guided, approach, or such interventions may prevent the conversion of MCI to dementia. The 12 risk factors used as an hypothetical intervention model were derived fro the 2020 Lancet publication titled "Dementia prevention, intervention, and care: 2020 report of the Lancet Commission."The 12 risk factors included in that study include:• Aim to maintain systolic BP of 130 mm Hg or less in midlife from around age 40 years (antihypertensive treatment for hypertension is the only known effective preventive medication for dementia).• Encourage use of hearing aids for hearing loss and reduce hearing loss by protection of ears from excessive noise exposure.• Reduce exposure to air pollution and second-hand tobacco smoke.• Prevent head injury.• Limit alcohol use, as alcohol misuse and drinking more than 21 units weekly increase the risk of dementia.• Avoid smoking uptake and support smoking cessation to stop smoking, as this reduces the risk of dementia even in later life.• Provide all children with primary and secondary education.• Reduce obesity and the linked condition of diabetes. Sustain midlife, and possibly later life physical activity.•Addressing other putative risk factors for dementia, like sleep, through lifestyle interventions, will improve general health. Lastly, the Lancet study concluded that "Modifying 12 risk factors might prevent or delay up to 40% of dementias."And, if you incorporate such risk reduction factors (there are more!) earlier in life, your odds of developing dementia in later years can be slashed even more dramatically.Think ahead!BrainDefend® ... See MoreSee Less

Personalized Alzheimer's Progression Predicted by Model

www.medpagetoday.com

Tool estimates how fast cognitive decline will occur in amyloid-positive patients

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THE ALZHEIMER'S SOLUTION

Testimonials

What 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!

Tim Walsh LAc

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.

Dr. Jones

Absolutely the BEST article I have read on the insulin/AD connection. As always, your brilliance is very much appreciated!

Kristin Rotblatt, L.Ac.

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.

Dr. Shah Roath

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A Personalized Body-Brain Health andRenewal Program designed to protectand optimize your cognitive health as you age.

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THE ALZHEIMER'S SOLUTION

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A Personalized Body-Brain Health and
Renewal Program designed to protect
and optimize your cognitive health as you age.