Fructose Metabolism in Alzheimer's Disease

The degree to which Alzheimer's disease is a lifestyle condition is an interesting question. A good deal of research points to insulin resistance in the brain as important in the progression of Alzheimer's disease, to the point at which one group declared Alzheimer's to be a type 3 diabetes, a condition that should be thought of as primarily metabolic in origin. That idea gained enough traction that when a definitively new type of diabetes was discovered, it had to be named type 4 diabetes to avoid confusion. Insulin resistance and type 2 diabetes are a consequence of being overweight in the vast majority of patients, but Alzheimer's disease isn't as obviously directly a consequence of excess fat as is the case for type 2 diabetes. Fewer overweight people develop Alzheimer's disease than develop type 2 diabetes - it isn't the same picture at all as the comparatively reliable progression to metabolic syndrome, insulin resistance, and then type 2 diabetes that happens as a result of excessive weight gain. Nonetheless, the disrupted metabolism of overweight people does look compelling as a contributing cause of this form of neurodegenerative condition. The loss of cognitive function in Alzheimer's disease is pathologically linked with neurofibrillary tangles, amyloid deposition, and loss of neuronal communication. Cerebral insulin resistance and mitochondrial dysfunction have emerged as important contributors to pathogenesis supporting our hypothesis that cerebra...
Source: Fight Aging! - Category: Research Authors: Tags: Daily News Source Type: blogs

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Fight Aging! publishes news and commentary relevant to the goal of ending all age-related disease, to be achieved by bringing the mechanisms of aging under the control of modern medicine. This weekly newsletter is sent to thousands of interested subscribers. To subscribe or unsubscribe from the newsletter, please visit: https://www.fightaging.org/newsletter/ Longevity Industry Consulting Services Reason, the founder of Fight Aging! and Repair Biotechnologies, offers strategic consulting services to investors, entrepreneurs, and others interested in the longevity industry and its complexities. To find out m...
Source: Fight Aging! - Category: Research Authors: Tags: Newsletters Source Type: blogs
In conclusion, it remains unclear if brain-specific regional and temporal changes occur in the expression of the different APP variants during AD progression. Since APP is also found in blood cells, assessing the changes in APP mRNA expression in peripheral blood cells from AD patients has been considering an alternative. However, again the quantification of APP mRNA in peripheral blood cells has generated controversial results. Brain APP protein has been analyzed in only a few studies, probably as it is difficult to interpret the complex pattern of APP variants and fragments. We previously characterized the soluabl...
Source: Fight Aging! - Category: Research Authors: Tags: Newsletters Source Type: blogs
I recently collaborated on a review paper covering the history of clinical work on upregulation of nicotinamide adenine dinucleotide (NAD) as an approach to therapy. This is of interest to the aging research community because NAD is important to mitochondrial function. NAD levels diminish with age, alongside a loss of mitochondrial function that is known to contribute to the onset and progression of many age-related conditions. Animal studies and a few clinical trials have indicated that increased NAD levels may improve, for example, cardiovascular function in older individuals, as a result of improved mitochondrial functi...
Source: Fight Aging! - Category: Research Authors: Tags: Medicine, Biotech, Research Source Type: blogs
In this study, we sought to elucidate the role of VRK-1 in regulation of adult life span in C. elegans. We found that overexpression of VRK-1::GFP (green fluorescent protein), which was detected in the nuclei of cells in multiple somatic tissues, including the intestine, increased life span. Conversely, genetic inhibition of vrk-1 decreased life span. We further showed that vrk-1 was essential for the increased life span of mitochondrial respiratory mutants. We demonstrated that VRK-1 was responsible for increasing the level of active and phosphorylated form of AMPK, thus promoting longevity. A Fisetin Variant, C...
Source: Fight Aging! - Category: Research Authors: Tags: Newsletters Source Type: blogs
In this study, we examined the effects of oxytocin on the Aβ-induced impairment of synaptic plasticity in mice. To investigate the effect of oxytocin on synaptic plasticity, we prepared acute hippocampal slices for extracellular recording and assessed long-term potentiation (LTP) with perfusion of the Aβ active fragment (Aβ25-35) in the absence and presence of oxytocin. We found that oxytocin reversed the impairment of LTP induced by Aβ25-35 perfusion in the mouse hippocampus. These effects were blocked by pretreatment with the selective oxytocin receptor antagonist L-368,899. Furthermore, the tr...
Source: Fight Aging! - Category: Research Authors: Tags: Newsletters Source Type: blogs
In this study, we applied a well studied prediction model developed on data from five CpG sites, to increase the practicability of these tests. We have determined the biological age of the heart, specifically of the right atrium (RA) and left atrium (LA), and of peripheral blood leucocytes, by measuring the mitotic telomere length (TL) and the non-mitotic epigenetic age (DNAmAge). We found that DNAmAge, of both atrial tissues (RA and LA), was younger in respect to the chronological age (-12 years). Furthermore, no significant difference existed between RA and LA, suggesting that, although anatomically diverse and ex...
Source: Fight Aging! - Category: Research Authors: Tags: Newsletters Source Type: blogs
This study was the first to demonstrate a causal relationship between glial senescence and neurodegeneration. In this study, accumulations of senescent astrocytes and microglia were found in tau-associated neurodegenerative disease model mice. Elimination of these senescent cells via a genetic approach can reduce tau deposition and prevent the degeneration of cortical and hippocampal neurons. Most recently, it was shown that clearance of senescent oligodendrocyte progenitor cells in AD model mice with senolytic agents could lessen the Aβ plaque load, reduce neuroinflammation, and ameliorate cognitive deficits. ...
Source: Fight Aging! - Category: Research Authors: Tags: Newsletters Source Type: blogs
This study provides direct evidence for the contribution of gut microbiota to the cognitive decline during normal aging and suggests that restoring microbiota homeostasis in the elderly may improve cognitive function. On Nutraceutical Senolytics https://www.fightaging.org/archives/2020/05/on-nutraceutical-senolytics/ Nutraceuticals are compounds derived from foods, usually plants. In principle one can find useful therapies in the natural world, taking the approach of identifying interesting molecules and refining them to a greater potency than naturally occurs in order to produce a usefully large therape...
Source: Fight Aging! - Category: Research Authors: Tags: Newsletters Source Type: blogs
In this study, we determine whether transient reintroduction of embryonic stem cell cycle miR-294 promotes cardiomyocyte cell cycle reentry enhancing cardiac repair after myocardial injury. A doxycycline-inducible AAV9-miR-294 vector was delivered to mice for activating miR-294 in myocytes for 14 days continuously after myocardial infarction. miR-294-treated mice significantly improved left ventricular functions together with decreased infarct size and apoptosis 8 weeks after MI. Myocyte cell cycle reentry increased in miR-294 hearts parallel to increased small myocyte number in the heart. Isolated adult myocytes from miR-...
Source: Fight Aging! - Category: Research Authors: Tags: Newsletters Source Type: blogs
Conclusions Two, Not Mutually Exclusive, Hypotheses We have reviewed and organized the literature with the intent of showing the existing parallels between excessive fat accumulation and the aging process. We have categorized these reports following what have been proposed to be the nine hallmarks of aging (21) (Figure 1). Based on the evidence, two distinct hypotheses can be proposed. One is that the cellular responses provoked by an excess of nutrients cause obesity, and that obesity is responsible for accelerating the pace of aging. Supporting this hypothesis are the observations that knocking out the fat-specific ins...
Source: Frontiers in Endocrinology - Category: Endocrinology Source Type: research
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