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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,...

Following nearly 10,000 older women for 10 years, researchers found that tea drinking was associated with slightly higher hip bone density. Moderate coffee consumption did not appear harmful, but drinking more than five cups a day was linked to lower bone density. The findings suggest tea may offer a small bone-health boost, while excessive coffee could carry some drawbacks.

Where you live in early adulthood may quietly shape your heart health for decades. Researchers found that adverse neighborhood conditions were linked to a higher risk of coronary artery calcification in midlife, an early warning sign of cardiovascular disease.

Obesity appears to leave a molecular imprint on key immune cells that may persist for 5 to 10 years after weight loss. This long-lasting “obesity memory” could help explain why some obesity-related health risks remain elevated even after body weight returns to normal.

Mindfulness, gratitude, and optimism training may improve blood pressure, inflammation, and other heart-health measures within just eight to 12 weeks. The strongest programs paired daily practice with regular reinforcement, suggesting that improving psychological well-being could become another tool for protecting cardiovascular health.