Each study has a usefulness score out of 100 (rubric version 4.0). Tap a score to see what makes it up.
Highest usefulness score first. Studies without a score come last.
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Accumulation and deposition of amyloid beta peptide (Abeta) in the brain causes neuronal apoptosis and eventually leads to Alzheimer's disease (AD).
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Sporadic Parkinson disease (PD) is, after Alzheimer disease (AD), the second most frequent neurodegenerative disorder.1 The pathologic process in PD is progressive and takes years to reach its full extent.
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We show that the glutathione pools in hepatic cells and in the blood are quite insensitive to fluctuations in amino acid input and offer an explanation based on model predictions.
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Intranasal insulin administration raises central nervous system (CNS) insulin levels in humans and acutely facilitates verbal memory in patients with Alzheimer's disease (AD), an effect that may differ by APOE genotype.
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A critical role of mitochondrial dysfunction and oxidative damage has been hypothesized in both aging and neurodegenerative diseases.
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A considerable literature has been published on the health benefits of fish, oil-rich fish and fish oils and their constituent long-chain (LC) n-3 PUFA.
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Reductions in cerebral metabolism sufficient to impair cognition in normal individuals also occur in Alzheimer's disease (AD).
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Cardiovascular disease and cancer are ranked as the first and second leading causes of death in the United States and in most industrialized countries.
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Alzheimer's disease affects nearly 5 million Americans currently and, as a result of the baby boomer cohort, is predicted to affect 14 million Americans and 22 million persons totally worldwide in just a few decades.
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The Abeta-amyloid peptide (Abeta), the main component of amyloid plaques, is derived by proteolytic cleavage from the amyloid precursor protein (APP).
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1. beta-Amyloid peptide (A beta), a 39 -- 43 amino acid peptide, is believed to induce oxidative stress and inflammation in the brain, which are postulated to play important roles in the pathogenesis of Alzheimer's disease.
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The central nervous system accounts for only 2% of the whole body mass but contains almost a quarter of the unesterified cholesterol present in the whole individual.
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Lipid peroxidation (LPO) is a free radical-related process that in biologic systems may occur under enzymatic control, e.g., for the generation of lipid-derived inflammatory mediators, or nonenzymatically.
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Decreases in mitochondrial respiratory chain complex activities have been implicated in neurodegenerative disorders such as Parkinson's disease, Huntington's disease, and Alzheimer's disease.
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40/100
Neurodegenerative diseases, in which neuronal cell disintegrate, bring about deteriorations in cognitive functions as is evidenced in millions of Alzheimer patients.
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The etiology of neurodegenerative diseases remains enigmatic; however, evidence for defects in energy metabolism, excitotoxicity, and for oxidative damage is increasingly compelling.
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Oxidative damage to DNA may play a role in both normal aging and in neurodegenerative diseases.
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Glucose metabolism is depressed in the temporal and parietal regions of the cortex in patients with Alzheimer's disease.
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In contrast, no increases in CSF QUIN were found in chronic neurodegenerative disorders, depression or myoclonic seizure disorders, while CSF kynurenic acid concentrations were significantly lower in Huntington's disease and Alzheimer's disease.
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The etiology of nerve cell death in neuronal degenerative disease is unknown, but it has been hypothesized that excitotoxic mechanisms may play a role.
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Quinolinic acid is an "excitotoxic" metabolite and an agonist of N-methyl-D-aspartate receptors.
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The purpose of this article is to highlight how sex differences in the gut-brain axis may contribute to the discrepancies in incidence of neurodevelopmental, psychiatric, and neurodegenerative disorders between females and males.
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39/100
Diabetes, obesity, and Alzheimer's disease (AD) are associated with vascular complications and impaired nitric oxide (NO) production.
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Common themes in the current literature include GMB components; interactions on cognitive development; effects of GMB-gut-brain interactions on cognition, mild cognitive impairment and Alzheimer's disease; effects of GMB interactions with physiologic stress on cognition in critical care; and GMB modification for improved cognition.
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The prevention or alleviation of neurodegenerative diseases, including Alzheimer's disease (AD), is a challenge for contemporary health services.
From across this topic
10 of the 1,048 studies in this topic, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
- Metabolic Network Analysis Reveals Altered Bile Acid Synthesis and Metabolism in Alzheimer's Disease
- Lipid peroxidation triggers neurodegeneration: a redox proteomics view into the Alzheimer disease brain
- Probiotics, gut microbiota, and brain health: Exploring therapeutic pathways
- Dietary Components and Nutritional Strategies for Dementia Prevention in the Elderly
- Insulin Signaling Impairment in the Brain as a Risk Factor in Alzheimer's Disease
- Microplastics-Induced Gut Microbiota Dysbiosis Accelerates Alzheimer's-Like Pathology and Cognitive Decline via the Gut-Brain Axis
- Gut microbiota, circulating cytokines and dementia: a Mendelian randomization study
- Gut feelings: the microbiota-gut-brain axis on steroids
- Urolithin A suppresses high glucose-induced neuronal amyloidogenesis by modulating TGM2-dependent ER-mitochondria contacts and calcium homeostasis
- Intestinal microbial dysbiosis aggravates the progression of Alzheimer's disease in Drosophila