Every article, presentation, spotlight, and news item we've tagged to Hallmarks of Aging.
Showing 49–72 of 232
p62 protein condensation drives clustering of damaged mitochondria during selective autophagy, acting as a quality control mechanism that slows mitochondrial turnover. ALS/FTD-associated mutations disrupt this clustering process, impairing the cell's ability to manage dysfunctional mitochondria—a hallmark of age-related neurodegeneration.
Oxidative damage biomarkers correlate with frailty in older women, providing measurable indicators of cellular stress that precede functional decline. Identifying these markers enables earlier intervention before frailty manifests clinically.
This research maps transcriptomic changes across multiple organs during aging in mice, revealing organ-specific and shared molecular signatures of senescence. Understanding these distinct aging patterns across tissues is fundamental to identifying intervention points for age-related decline.
ATP deficiency impairs dopamine packaging into synaptic vesicles by reducing function of VMAT2, a transporter that requires ATP energy, leading to dopamine oxidation and α-synuclein accumulation characteristic of Parkinson's disease. This mechanism links mitochondrial dysfunction to neurodegeneration in human dopaminergic neurons and may explain both familial and sporadic disease pathology.
Microbiota from elderly donors with both Alzheimer's disease and type 2 diabetes produce the most severe dysbiosis when transplanted into mice, suppressing hippocampal neurotrophic gene expression through loss of butyrate-producing bacteria and enrichment of pro-inflammatory taxa. This demonstrates a direct mechanistic link between comorbid metabolic and neurodegenerative disease states and gut-brain axis dysfunction.
This issue of Aging Cell (Volume 25, Issue 4, April 2026) aggregates current research on cellular and organismal aging mechanisms. Without access to specific article abstracts or contents, the longevity relevance depends on the individual research papers included in this issue.
This correction addresses a published study on how senescent cells reorganize their chromatin architecture in response to therapeutic stress. Understanding the structural changes in non-dividing cells has direct implications for improving cellular resilience and longevity through better therapeutic design.
Anavex presents evidence linking autism spectrum disorder and Alzheimer's disease through impaired autophagy and synaptic dysfunction, proposing that restoring cellular clearance pathways via their compound Blarcamesine may address both conditions. The finding connects neurodevelopmental and neurodegenerative disease through a shared cellular mechanism, with epidemiological data showing autistic adults face substantially elevated dementia risk.
Ternary Therapeutics raised $4.4 million to develop AI-designed molecular glues that selectively degrade or modulate proteins driving chronic inflammation and neuroinflammation. This approach addresses inflammaging, a fundamental aging process linked to age-related disease burden, through a closed-loop AI platform rather than conventional blocking mechanisms.
Single-cell analysis reveals that aging bone marrow undergoes distinct cellular remodeling: endothelial cells develop prothrombotic and mitochondrial dysfunction, while a novel RAB13+ arterial endothelial subset emerges alongside expansion of profibrotic mesenchymal cells. These cellular shifts directly impair the marrow's capacity to support healthy blood cell production and tissue maintenance, establishing specific molecular targets for intervention.
Senescent hepatocytes in aging release extracellular vesicles containing microRNAs that enhance metastatic potential across multiple cancer types in aged organisms. This mechanism directly links hepatic aging to systemic cancer progression, identifying a previously uncharacterized pathway connecting liver dysfunction to increased metastatic risk in older adults.
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.
Senescent cells accumulate with age and suppress antiviral immunity through four secreted factors—GDF15, IGF1, IL1α, and IL6—via two distinct signaling pathways. Blocking these factors restores innate antiviral defense in aged mice, offering a mechanistic target to improve immune resilience against infection in older adults.
Intervertebral discs age slowly due to selective autophagy of HIF-1α under naturally hypoxic conditions. A small molecule designed to replicate this mechanism across tissues may extend mammalian lifespan by modulating how cells respond to low-oxygen environments.
Specific dietary metabolites—compounds produced when the body processes food—predict frailty risk through inflammatory pathways in aging adults. This identifies measurable intermediate markers that connect diet composition to loss of physical function, a primary driver of morbidity and mortality in older populations.
Mendelian randomization analysis demonstrates that elevated IL-6, a pro-inflammatory cytokine, causally increases mortality risk, while circulating IL-6 receptor (IL6R) decreases it. This identifies a specific inflammatory pathway amenable to therapeutic intervention in age-related mortality.
Gene expression analysis of human hippocampal tissue reveals distinct molecular signatures in aging characterized by increased inflammation, reduced DNA repair capacity (particularly RAD23B), and altered neural activity patterns. RAD23B expression declines with age and is further reduced in Alzheimer's disease, positioning it as a relevant marker of hippocampal aging and neuronal vulnerability.
Single-cell immune profiling across nearly 1,000 adults reveals sex-specific patterns of immune aging, with females demonstrating more extensive age-related remodeling of immune function. These findings establish a biological basis for observed sex differences in inflammatory disease prevalence and infection susceptibility across the lifespan.
Microglia—the brain's resident immune cells—exhibit distinct transcriptional patterns and morphological changes with age, with subcellular mRNA localization directly influencing their functional capacity. This work establishes how aging alters the molecular foundation of neuroinflammation, a process central to cognitive decline and neurodegenerative disease progression.
This correction addresses methodological refinements in research demonstrating that monoamine oxidase-A drives stress-induced cellular aging by disrupting the cell's ability to clear damaged mitochondria. The finding clarifies a direct mechanism linking stress response dysfunction to accelerated senescence at the mitochondrial level.
Telomere shortening drives atrial fibrillation through VCAM-1 upregulation, which promotes atrial fibrosis and electrical dysfunction. Blocking VCAM-1 reverses these changes and reduces AF susceptibility by 30%, identifying a mechanistic pathway linking cellular aging to arrhythmia risk.
Pck1 deficiency in adipocytes impairs mitochondrial function, causing fumarate accumulation that triggers oxidative stress, mtDNA release, and chronic inflammation—a mechanism linking metabolic dysfunction to aging. This identifies a targetable pathway in the progression of age-related metabolic disease.
Oxidative stress in oocytes from aged female mice triggers lipid accumulation and metabolic alterations that persist through three generations, with offspring developing compensatory antioxidant responses in lipid-rich tissues. This demonstrates that maternal aging imprints metabolic dysfunction on descendants independent of direct genetic mutation.
Jeremy Walston's work established frailty as a biologically coherent condition rooted in chronic inflammation, mitochondrial dysfunction, and impaired stress responsiveness rather than inevitable aging. His translational research framework has advanced clinical intervention strategies and shaped how geroscience addresses loss of physiologic reserve across aging populations.
