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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Mitochondrial dysfunction, oxidative stress, neuroinflammation, and impaired protein homeostasis form interconnected pathological networks in acute central nervous system injury and chronic neurodegenerative disease.
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Sulforaphane (SFN), a natural isothiocyanate from cruciferous vegetables, exerts neuroprotective effects through mechanisms extending beyond canonical Nrf2/ARE activation.
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Alzheimer’s disease (AD) is a progressive, neurodegenerative disorder and the leading cause of dementia worldwide.
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Butyrate, a 4-carbon fatty acid produced from insoluble starch by the gut microbiome, plays key roles in mitochondrial respiration, activation of cell-surface G-protein-coupled receptors, and protein acetylation by inhibiting histone deacetylases (HDACs).
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Neurodegenerative diseases are a growing global health burden associated with aging and characterized by progressive neuronal dysfunction, metabolic failure, mitochondrial impairment, oxidative stress, and chronic neuroinflammation.
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Maternal microbiome-dependent programming of neuroimmune and metabolic pathways during early development may critically shape sex-specific susceptibility to Alzheimer’s disease (AD) later in life.
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Alzheimer’s disease (AD) affects women more than men, with risk increasing during and after the menopausal transition.
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Early Ap accumulation is associated with distinct gut microbial signatures and reduced neuroactive metabolic potential, identifying targets for potential preclinical AD intervention.
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Mitochondrial dysfunction is a shared biological thread between terrestrial Alzheimer’s disease (AD) and in the unique stress environment of spaceflight, making mitochondrial pathophysiology a compelling target for comparative investigation.
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Intranasal insulin has been investigated as a metabolic intervention in Alzheimer’s disease (AD), but its effects across the brain–gut axis remain unclear.
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Alzheimer’s disease (AD) involves widespread metabolic, mitochondrial, inflammatory, and redox dysfunction.
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These integrated findings support H. erinaceus as a candidate adjunct to donepezil, with possible complementary effects on amyloidogenic processing and intracellular clearance.
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Most included studies were purely in vitro (n = 18); six combined in vitro and in vivo methods, and two used in vitro and in silico or ex vivo components.
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Spermine exerts neuroprotective effects in VaD by inhibiting TRPM2-mediated oxidative stress and activating the Nrf2/SLC7A11/GPX4 pathway, thereby suppressing ferroptosis.
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Although endoplasmic reticulum (ER) stress and maladaptive unfolded protein response (UPR) are increasingly implicated in Alzheimer’s disease (AD), the influence of vitamin D (VitD) on these mechanisms remains unclear.
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Frailty index was associated with carboxylic acids and derivatives, fatty acyls and organooxygen compounds across multiple clusters, and a large number of lipids were linked to frailty score, potentially implicating dysregulation of energy metabolism in the pathophysiology of frailty and forming a panel of predictive biomarkers of at risk patients.
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However, increasing evidence indicates that systemic metabolic dysfunction, chronic inflammation, intestinal dysbiosis, hepatic abnormalities, and barrier impairment may substantially influence disease susceptibility and progression.
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The glycolytic regulator PFKFB3 supports dysfunctional β-cell states, but its role in pancreatic Ca 2+ signaling remains unclear.
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Traumatic brain injury (TBI) is a risk factor for Alzheimer’s disease (AD), and both conditions are associated with impaired glucose metabolism and mitochondrial dysfunction.
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Environmental exposures are major but understudied determinants of chronic disease.
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Public interest in cannabinoid medicines has outpaced the clinical pharmacology needed to judge product, dose and route.
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Alzheimer’s disease (AD) is a neurodegenerative disorder characterized primarily by progressive cognitive impairment.
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Apigenin is an abundant, bioactive phytochemical with reported therapeutic potential and neuroprotective effects in a variety of age-related disease models.
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Physical exercise promotes systemic and neural adaptations that support healthy brain aging and may mitigate Alzheimer’s disease (AD) progression.
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Galantamine is a pharmaceutically relevant Amaryllidaceae alkaloid used for the treatment of Alzheimer’s disease.