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“Broken heart syndrome” can mimic a heart attack so closely that patients often need invasive testing to tell the difference. Researchers have now developed the BioTAK score, which combines biological sex with blood biomarkers to identify the condition before cardiac catheterization. In a validation study of nearly 1,800 patients, it correctly classified almost 90% of participants.

Persistent financial hardship in early and middle adulthood was linked to poorer thinking skills by the 50s and more signs of brain aging later in life. Researchers say years of chronic stress and financial worry may gradually take a toll on the brain.

Brain changes associated with Alzheimer’s may begin at least seven years before amyloid plaques become detectable with current PET scans. Researchers uncovered the signal by tracking healthy older adults with repeated brain imaging over nearly 20 years. The discovery could help scientists identify Alzheimer’s earlier and suggests that important disease processes may start before visible plaque buildup.

CONCLUSION: Iron deposition in the PUT exhibits the most significant age dependence; the correlation of iron deposition among nuclei may indicate that specific nuclei share the same iron deposition patterns or are involved in the same pathological mechanisms.

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CONCLUSION: A first fall report marked a period of accumulating physiological, psychological, and functional vulnerability in both cohorts. Because time zero was a survey report wave rather than the exact fall date, these event-aligned associations do not isolate acute causal effects. Nevertheless, a first fall report may provide a useful trigger for comprehensive assessment and sustained functional support.

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Symptomatic treatment remains central to the clinical management of Alzheimer disease (AD), even as disease-targeted therapies emerge. This Review synthesizes current evidence for pharmacological and non-pharmacological symptomatic therapies targeting cognition, function and neuropsychiatric symptoms in AD. Non-pharmacological interventions, including cognitive training, physical exercise, cognitive stimulation therapy and multimodal lifestyle programmes, show small-to-moderate benefits,...

The study of Alzheimer's disease (AD)-associated mutations has implicated dysregulation of amyloid precursor protein (APP) proteolysis in the disease. Brain recordings have revealed synaptic hyperexcitation during asymptomatic and early stages of AD, reverting to overinhibition as dementia progresses. Here, we show that endogenous APP and its proteolytic C-terminal fragments (APP-CTFs), the precursors of amyloid-β (Aβ), are enriched at excitatory synapses. Pharmacological modulation of...

Damaged mitochondria are selectively eliminated through mitophagy, a critical quality control process. A kinase PINK1 and an E3 ubiquitin ligase PRKN/Parkin, both of which are mutated in familial Parkinson disease, amplify ubiquitin signals on the damaged mitochondria. The autophagy receptor OPTN plays a pivotal role in mitophagy by bridging ubiquitinated mitochondria with autophagy components. Although OPTN is known to recruit ATG9A-positive vesicles to facilitate mitophagy progression, the...

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Cellular senescence, a hallmark of aging, entails the irreversible cessation of cell division in response to intrinsic and extrinsic stressors. Though metabolically active, senescent cells lose their replicative capacity and resist apoptotic signals, accumulating tissues with advancing age and contributing to age-related pathologies. Senescence is characterized by the acquisition of a senescence-associated secretory phenotype (SASP), releasing a myriad of bioactive molecules. SASP not only...

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Naturally aged mice provide an important platform for studying frailty because functional decline emerges during biological aging rather than through acute injury or artificial manipulation. This review critically examines major frailty assessment tools used in aged mice, including the mouse frailty index, mouse frailty phenotype, physical function score/vitality score, mouse social frailty index, and mouse cognitive frailty index. We compare their conceptual foundations, scoring procedures,...

Aged skeletal muscle is impaired at every phase of post-injury repair that has been examined, with myeloid recruitment delayed and skewed in composition, debris degradation lagging behind uptake, and muscle stem cell (MuSC) activation following a conserved trajectory at delayed kinetics. Deficits inside a phase may be differences of degree that a longer window absorbs, whereas the transition between phases offers no comparable slack. Each transition is triggered by a defined switch in signal,...