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Metabolic Pathways

Metabolic Pathways Library

Every article, presentation, spotlight, and news item we've tagged to Metabolic Pathways.

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Showing 73–81 of 81

Wiley Aging CellFeb 25, 2026

Silencing of the Metabolic Gene HKDC1 Is Associated With Aging and Neurodegeneration in Mice and Humans

HKDC1, a metabolic enzyme, declines with age due to chromatin remodeling that blocks its transcription factor regulation, and this decline correlates with cognitive impairment and neurodegeneration in both mice and humans. Loss of HKDC1 compromises mitochondrial integrity and triggers neuroinflammation, establishing a mechanistic link between metabolic gene silencing and age-related neurological decline.

Wiley Aging CellMar 20, 2026

FGF21‐Mediated Upregulation of SIRT1 Delays Intervertebral Disc Degeneration by Promoting PINK1/Parkin Dependent Mitophagy Through Deacetylation of FOXO3

FGF21 activates a cellular repair pathway in spinal disc cells by upregulating SIRT1, which deacetylates FOXO3 and triggers mitochondrial autophagy, thereby suppressing cell senescence and slowing intervertebral disc degeneration. This identifies a targetable molecular axis with direct relevance to preventing age-related spinal structural decline and associated disability.

LifeSpan.ioApr 15, 2026

Vitamin C Alleviates Aging in Cynomolgus Monkeys

Iron accumulation drives a coordinated aging process called ferro-aging through oxidative damage and lipid peroxidation; vitamin C reverses these markers in primate models. This identifies iron metabolism and lipid oxidation as actionable targets in cellular senescence.

LifeSpan.ioFeb 13, 2026

Cellular Reprogramming Rescues Memory-Encoding Neurons

Partial cellular reprogramming using three Yamanaka factors (OSK) successfully restored memory function in aged mice and Alzheimer's disease models by rejuvenating memory-encoding neurons while preserving their neuronal identity. This approach demonstrates that targeted reprogramming of engram cells can reverse age-related cognitive decline without causing dedifferentiation or memory loss.

Wiley Aging CellMar 30, 2026

Autophagy‐Independent Function of ATG‐18 Is Essential for Gonadal Longevity in Caenorhabditis elegans

ATG-18, a protein long associated with autophagy, extends lifespan through a mechanism independent of autophagy itself when the germline is removed. In the intestine, ATG-18 extends lifespan by interacting with PCK-2, an enzyme involved in glucose production, revealing a tissue-specific, non-autophagic pathway to longevity.

LifeSpan.ioApr 15, 2026

Vitamin C Alleviates Aging in Cynomolgus Monkeys

Iron accumulation drives a coordinated aging process termed ferro-aging, characterized by oxidative damage and cellular senescence across tissues. Vitamin C administration reversed aging markers and restored functional capacity in aged cynomolgus monkeys, suggesting a tractable intervention point in iron-dependent aging pathways.

Longevity.TechnologyMar 3, 2026

Higher tyrosine levels may trim years off life

A UK Biobank study of 272,500 participants links elevated blood tyrosine levels to reduced lifespan, with a stronger effect in men (approximately one year lost per standard deviation increase). Using Mendelian randomization to establish causality rather than mere association, the research suggests tyrosine acts as a causal factor in mortality risk, independent of phenylalanine.

Nature - npj AgingMar 13, 2026

Multifunctionality of TIM-3: from immunological aging to pathological progression

TIM-3, an immune checkpoint protein, drives age-related immune dysfunction and contributes to neurodegeneration and brain tumors through promotion of immunosuppressive myeloid cells. Blocking TIM-3 represents a potential therapeutic approach to restore immune competence in central nervous system disease.

Longevity.TechnologyMar 19, 2026

Targeting protein misfolding in neurodegeneration

Protein misfolding drives over 100 diseases and accelerates aging-related decline. Origami Therapeutics is developing targeted protein degraders and conformation correctors that address root cause mechanisms rather than symptoms, with initial focus on neurodegenerative diseases including Huntington's, Alzheimer's, and Parkinson's.