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How COVID-19 might increase risk of memory loss and cognitive decline
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
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
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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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 were lost, it was a fait accompli. Damaged neurons were considered damaged goods, never to regain their ...
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#senotherapeutics #cellularsenescense #alzheimersrisk![]()
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In my last post here, I described and passed on research that detailed the role of a type of programmed cell death process—ferroptosis—that is initiated by iron overload and oxidative stress.![]()
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The dysregulation of such normal programmed cell death (PCD) pathways are a significant component to accelerated aging and age-related diseases including cancer, cardiovascular diseases and neurological diseases such as Alzheimer's. ![]()
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Similarly, as we age senescent cells (cellular senescence) of the body and brain come to an arrested and irreversible point in the cell cycle (stages of growth, DNA synthesis, and cell division)—an endpoint in their lifespan—whereupon the senescent cell is normally removed by the immune system or through a PCD pathway.![]()
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Additionally, in age-related diseases such as Alzheimer's and cardiometabolic disease, pro-inflammatory and oxidative cellular stress mechanisms leads to premature cellular senescence.![]()
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However, in a state of cellular senescence, senescent immune system cells also fail to perform their senescent cell removal and disposal as they also accumulate (immunosenescence).![]()
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Apart from the normal immune system clearance of senescent cells, a programmed cell death pathway known as apoptosis (not ferroptosis), is an additional mechanism for senescent cell removal.![]()
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However, instead of a normal cell death and elimination, senescent cells resist apoptosis (apoptotic resistance) and remain alive—sort of and not in a good way.![]()
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These lingering senescent cells are now popularly referred to as "zombie cells". ![]()
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The problem with senescent or zombie cells is they accumulate and secrete multiple inflammatory proteins which creates a toxic milieu that spreads havoc to neighboring cells and actively promote tissue deterioration.![]()
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Such a toxic cellular environment is coined the senescence-associated secretory phenotype (SASP).![]()
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The SASP has been directly implicated as a key driver of aging and age-related diseases.![]()
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What to do?![]()
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The growing field and science of aberrant cellular senescence and the SASP has led to the understanding that there are tools for removing these arrested and toxic cell senescent cells which is termed—senolysis—the selective elimination of senescent cells.![]()
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Induction of senolysis has emerged as "senolytic" therapy (senotherapeutics) approach that is promoted by several senolytic compounds including repurposed drugs (e.g. dasatinib), and natural agents such as polyphenols (e.g., fisetin, quercetin) that are well-studied senolytic agents. ![]()
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How do these wonder polyphenolic compounds that are abundant in a health diet work ? ![]()
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Through the induction of apoptosis and the support of a healthy immune system which inhibits immunosenescence.![]()
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The link here gets you to the review of a Wake First University report of a small—5 participants —12 week phase 1 feasibility trial results that showed the combined efficacy of dasatinib and quercetin in clearing "senescent brain cells in Alzheimer’s disease mouse models".
newsroom.wakehealth.edu
Alzheimer’s disease is the most common cause of dementia that affects more than 6.5 million Americans, according to the Alzheimer’s Association.
#ferroptosis #alzheimersrisk #vasculardementia![]()
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Senescent and diseased cells are destroyed and disposed of by three types of programmed cell death—apoptosis (type 1 cell death), autophagic cell death (type 2), and necrosis (type 3).![]()
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The mechanisms underlying these programmed cell death pathways are a critical component in maintaining cellular homeostasis in aging, and in the prevention of diseases.![]()
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There is also another form of programmed cell death, ferroptosis (non-apoptotic), that has recently emerged as the focus of many studies after it was first described in a 2012 paper.![]()
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Ferroptosis is characterized and triggered by intracellular accumulation of iron and reactive oxygen species (ROS), and has been linked to the progression of several diseases, including cancers, cardiovascular diseases, neurological diseases, and renal disease.![]()
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In aberrant ferroptosis, dysregulation of the programmed cell death pathway associated with cellular iron overload and increased ROS that leads to lipid peroxidation, are a significant component of such diseases.![]()
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In neurological diseases such as Alzheimer's and vascular dementia, the brain's immune cells, microglia, attempt to clear away the lipid-rich myelin sheath that envelops the cells axon extensions, which is damaged by oxidation (lipid peroxidation).![]()
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However, in aberrant ferroptosis the vital protective microglia are also damaged and eventually destroyed.![]()
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What creates this ferroptosis associated toxic iron and ROS overload that disrupts the regulated cell pathways which are critical to maintaining cellular homeostasis and the prevention of Alzheimer's disease and vascular dementia?![]()
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As I describe in my book, The Diabetic Brain in Alzheimer's Disease, years of chronic inflammation and oxidative stress pathways associated with type 2 diabetes and cardiovascular disease (cardiometabolic disease), puts your brain at significant risk for dementia and Alzheimer's disease later in life.![]()
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Think ahead!![]()
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BrainDefend ® ![]()
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Iron Buildup Triggers Cell Death in Alzheimer's - Neuroscience News
neurosciencenews.com
Researchers identified a new form of cell death, termed ferroptosis, in Alzheimer’s disease and vascular dementia.
#betaamyloidandtauprotein #bloodtest #alzheimersrisk![]()
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"C₂N Diagnostics Releases the PrecivityAD2™ Blood Test for Clinical Care, A Robust Assay with High Concordance to Amyloid PET and CSF"![]()
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On the heels of the recent announcement by Quest Diagnostics that their blood beta-amyloid test (AD Detect) was now available to the public, C₂N Diagnostics has announced that their innovative PrecivityAD2™ blood test has been launched.![]()
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C₂N is a molecular diagnostics company, and their new PrecivityAD2™ blood test is a step up on their PrecivityAD™ blood test.![]()
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Apart from the beta-amyloid 42/40 ratio assessment and ApoE genotype profiling included in the PrecivityAD™ blood test, PrecivityAD2™ adds another set of significant blood biomarkers—phosphorylated and nonphosphorylated forms of the p-tau217 and p-tau181 proteins.![]()
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The ApoE genotyping profile, however, is not included with PrecivityAD2™.![]()
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The PrecivityAD2™ beta-amyloid and tau ratio assessments “are combined into a proprietary statistical algorithm to calculate the Amyloid Probability Score 2 (APS2)”, which is an indicator of whether a patient has a high or low probability of the presence of brain amyloid plaques by PET neuroimaging scan.![]()
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The APS 2 score was developed by C₂N 's proprietary algorithm, and an independent study recently published demonstrated that APS2 was a valid and accurate indicator of amyloid pathology.*![]()
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Undoubtedly, in the hands of a skilled clinician, the PrecivityAD2™ will now make available to authorized healthcare providers a blood test* with high diagnostic accuracy* in detecting Alzheimer’s disease pathology, and will enable an early assessment approach for individuals with MCI and more severe cognitive impairment.![]()
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Adding an ApoE genotype profile assessment to PrecivityAD2™ will further support a clinical assessment and evaluation.![]()
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Several recent and independent studies have shown that p-tau217 and and p-tau218 had “excellent diagnostic performance for differentiating patients with Alzheimer's disease syndromes from other neurodegenerative disorders”,** and a recent study concluded that “were highly specific for amyloid plaque pathology”.***![]()
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Contact information for C₂N is included in the link here."![]()
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c2n.com/news-releases/cnnbspdiagnostics-releases-the-precivityad2-blood-test-for-clinical-care![]()
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*Independent study demonstrates amyloid probability score accurately indicates amyloid pathology. ![]()
Fogelman I, West T, Braunstein JB, Verghese PB, Kirmess KM, Meyer MR, Contois JH, Shobin E, Ferber KL, Gagnon J, Rubel CE, Graham D, Bateman RJ, Holtzman DM, Huang S, Yu J, Yang S, Yarasheski KE.![]()
Ann Clin Transl Neurol. 2023 May;10(5):765-778. ![]()
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**Advancing Research and Treatment for Frontotemporal Lobar Degeneration investigators. Plasma phosphorylated tau 217 and phosphorylated tau 181 as biomarkers in Alzheimer's disease and frontotemporal lobar degeneration: a retrospective diagnostic performance study. ![]()
Thijssen EH. et al.,![]()
Lancet Neurol. 2021 Sep;20(9):739-752.![]()
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***Blood plasma phosphorylated-tau isoforms track CNS change in Alzheimer’s disease![]()
Barthelemy et al.![]()
J Exp Med (2020) 217 (11): e20200861.![]()
doi.org/10.1084/jem.20200861
#betaamyloid #bloodtest #alzheimersrisk![]()
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Not surprisingly, a number of Alzheimer's advocacy groups, physicians and the Alzheimer's Association raised concerns with regard to the plasma beta-amyloid blood test—Quest AD Detect—from Quest Diagnostics.![]()
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Please read the previous post here with regard to Quest's AD Detect announcement.![]()
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The concerns expressed in the MedPage Today report linked to here are valid, including lack of FDA approval and insurance coverage restrictions if there are findings of lower Aβ42/40 ratio that may correlate to an early stage (preclinical) of Alzheimer's disease (asymptomatic), or a higher risk of developing Alzheimer's disease (AD) in later years.![]()
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Another perspective:![]()
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If you recall, in November-2020, and after years of coming soon teasers, the eagerly anticipated announcement for the first beta-amyloid blood test for clinical use was made.![]()
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It was a welcomed report of a clinically validated test that was not criticized as Quest's AD Detect public offering is now. and a less expensive and invasive test to cerebrospinal fluid and neuroimaging assessments.![]()
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As the report linked to here also notes, many physicians do not understand how to interpret and proceed with such findings as which may be a much more significant concern.![]()
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Nevertheless, in the hands of an experienced neurologist or integrative physician with training in how to evaluate and guide patients that are deemed at higher risk for AD, the AD-Detect test along with other evaluations that includes a thorough family history analysis, these RISK evaluations, which are NOT intended to be diagnostic, can be extremely useful in a proactive and prevention-minded approach in an Alzheimer's risk reduction strategy.![]()
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Note that there are other resources and evaluations for plasma biomarkers that may correlate to a higher risk for AD.![]()
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The plasma Aβ42/40 ratio assessment has been vetted in many studies* and it's integration into other Alzheimer's risk analysis assessments has been encouraged in cognitively impaired AND unimpaired individuals. In the latter, it may serve to intervene much earlier in the disease process and hopefully halt its progression to a diagnosis of dementia.![]()
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**Recently, blood test reports for plasma tau protein (phospho-Tau217) have shown significant promise for adjunctive assessment options to the Aβ42/40 ratio assessment.![]()
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Such plasma tau protein tests are available to physicians.![]()
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Additionally, neuroimaging tests such as PET, MRI and SPECT are accepted as valuable adjunctive tools for a biomarker guided approach for early diagnosis and treatment.![]()
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In combination with genetic profiling, cardiometabolic risk assessments, evaluations for hormone imbalances and deficiencies, and cognitive performance tests and others, such evaluations can also shed light on person's risk and vulnerability for LOAD as they age.![]()
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Don't wait to be diagnosed. ![]()
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* Assessment of Plasma Amyloid-β42/40 and Cognitive Decline Among Community-Dwelling Older Adults. ![]()
Giudici KV, de Souto Barreto P, Guyonnet S, Li Y, Bateman RJ, Vellas B; MAPT/DSA Group.![]()
JAMA Netw Open. 2020 Dec 1;3(12):e2028634.![]()
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**Plasma phosphorylated tau 217 in preclinical Alzheimer’s disease.![]()
Erin M. Jonaitis, Shorena Janelidze, Karly A. Cody, Rebecca Langhough, Lianlian Du, Nathaniel A. Chin, Niklas Mattsson-Carlgren, Kirk J. Hogan, Bradley T. Christian, Tobey J. Betthauser, Oskar Hansson and Sterling C. Johnson![]()
Brain Communications. March 2023, 5(2)
Quest's Alzheimer's Blood Test Has Experts Concerned
www.medpagetoday.com
'Patients will have a difficult time knowing what the results mean'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.