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Bioengineering strategies to interrogate and modulate the aging immune system
40,000-year-old bird carvings provide clues to how ice age humans flourished
Obituary: Susumu Tonegawa, Japan’s first Nobel prizewinner in physiology or medicine
Polio will come roaring back if the task of eradicating it isn’t finished soon
Papers with open peer-review reports are less likely to be retracted
Misfolded insulin may be quietly driving diabetes
Researchers found that insulin-producing cells depend on a team of helper proteins to keep insulin production on track. When one key partner was missing, damaged proteins built up and the cells made less insulin. Strengthening this system could offer a new way to protect the pancreas as diabetes progresses.
Gene may help lizards get a grip in hurricane-force winds
“Huge” new study of Caribbean anole populations catches evolution in real time
Why losing weight may not be enough to prevent type 2 diabetes
A healthy lifestyle can prevent type 2 diabetes for many people, but new research suggests that weight loss alone may not be enough for one particularly vulnerable group. Even after losing about 8% of their body weight and keeping it off for years, people in a high-risk category known as cluster 5 continued to experience rising blood sugar, weakening insulin production, and a strong risk of developing diabetes.
Parent-of-origin effects in Alzheimer's liability dissociate neurocognitive and cardiovascular traits in at-risk individuals
Alzheimer's disease (AD) has a higher prevalence in women than men and is more frequently inherited from mothers than fathers. Yet, while neuroimaging and biomarker studies link maternal family history to stronger AD-related alterations, epidemiological studies suggest that paternal history confers comparable or even greater risk. Here, we leverage the deeply profiled PREVENT-AD cohort to derive three intermediate phenotypes of AD susceptibility. Drawing on nearly 1,000 individual study visits,...
Non-transgenic rodent models associated with Alzheimer's disease: applications, evaluation, and perspectives
Alzheimer's disease (AD) is a progressive neurodegenerative disorder. Familial AD accounts for less than 1% of cases, while sporadic AD (SAD) accounts for over 95%. Mild cognitive impairment (MCI) is the critical transition phase from normal aging to AD dementia. Understanding the pathological progression from MCI to AD and the mechanisms underlying SAD is essential. Rodent models, including transgenic and non-transgenic models, are vital tools for developing effective AD therapies. However,...
The Human Retina in Alzheimer's Disease: Pathology, Mechanisms, and Biomarkers
Alzheimer's disease (AD) is characterized by progressive neurodegeneration and synaptic dysfunction that begins decades before clinical symptoms emerge. While AD research has traditionally focused on the brain, increasing evidence suggests that the retina undergoes pathological remodeling that shares features with cerebral changes. Advances in retinal imaging, including optical coherence tomography (OCT), OCT angiography, and hyperspectral approaches, have identified structural, vascular, and...
Gating of Somatosensory Neural Oscillations Across the Lifespan: A Narrative Review
Healthy and pathological aging are associated with progressive changes in cortical inhibition, yet the underlying neural mechanisms remain incompletely understood. Somatosensory gating (SG), the brain's suppression of redundant tactile input, provides a pre-attentive marker of inhibitory function. Paired-pulse paradigms concurrent with noninvasive magnetoencephalography (MEG) provide a millisecond portrayal of the neural dynamics underlying somatosensory processing and the gating of such...
Is amyloid beta peptide a driver of inflammaging?
Inflammaging, the chronic subclinical systemic inflammation accompanying aging, represents a critical pathogenetic mechanism underlying age-related neurodegenerative diseases. While amyloid beta (Aβ) peptides are established contributors to neuroinflammation in Alzheimer's disease, their role in aging-related subclinical inflammation remains insufficiently elucidated. In humans, Aβ exhibits dual functions: it supports neuronal activity, survival, and protection against neurotrauma, while also...
Modernizing cognitive assessment in Alzheimer's disease
No abstract
Chromatin topology and distal elements underlie divergent cell-type-specific regulation of 9p21 locus cell cycle genes
The 9p21 locus encodes critical cell cycle regulators p16^(INK4A), p14^(ARF), and p15^(INK4B) and contains a high density of SNPs associated with aging-related diseases. Progress toward understanding 9p21 regulatory mechanisms has been constrained by complex transcript structures and a shortage of cell models that retain physiologic locus control. We innovated tools to deconvolve the expression and regulation of 9p21 transcripts in single cells. We find that 9p21 transcripts exhibit highly...
Non-transgenic rodent models associated with Alzheimer's disease: applications, evaluation, and perspectives
Alzheimer's disease (AD) is a progressive neurodegenerative disorder. Familial AD accounts for less than 1% of cases, while sporadic AD (SAD) accounts for over 95%. Mild cognitive impairment (MCI) is the critical transition phase from normal aging to AD dementia. Understanding the pathological progression from MCI to AD and the mechanisms underlying SAD is essential. Rodent models, including transgenic and non-transgenic models, are vital tools for developing effective AD therapies. However,...
Myokines as molecular mediators of the muscle-brain axis: Mechanisms linking sarcopenia to cognitive decline and implications for preventive strategies in ageing - A narrative review
Sarcopenia and cognitive decline frequently co-occur in older adults, and growing evidence indicates that these conditions share a common biological substrate centred on the muscle-brain axis. In this narrative review we synthesise contemporary mechanistic and translational evidence on how skeletal muscle communicates with the ageing brain through myokines and exerkines - including irisin/FNDC5, brain-derived neurotrophic factor (BDNF), interleukin-6 (IL-6), insulin-like growth factor-1 (IGF-1),...
Complosome as a key modulator of cellular senescence, aging and age-related diseases
Aging is characterized by progressive physiological decline and accumulation of senescent cells that drive chronic "inflammaging" through the senescence-associated secretory phenotype (SASP). The complement system, traditionally viewed as a systemic extracellular defense mechanism, is now recognized as an essential intracellular network (the complosome). This review synthesizes current research on how intracellular C3 (intC3), and intracellular C5 (intC5) in certain contexts engage in extensive...
From Primates to People: Mapping Host-Microbiome-Health Relationships in Aging
The human microbiome profoundly influences host physiology, metabolism, and immune function. A balanced microbial ecosystem supports immune homeostasis and health, whereas dysbiosis contributes to diverse diseases, including metabolic, autoimmune, neurodegenerative, and infectious disorders. Aging, the greatest risk factor for chronic disease, is characterized by hallmarks such as mitochondrial dysfunction, genomic instability, and "inflammaging," a state of chronic low-grade inflammation....
Gating of Somatosensory Neural Oscillations Across the Lifespan: A Narrative Review
Healthy and pathological aging are associated with progressive changes in cortical inhibition, yet the underlying neural mechanisms remain incompletely understood. Somatosensory gating (SG), the brain's suppression of redundant tactile input, provides a pre-attentive marker of inhibitory function. Paired-pulse paradigms concurrent with noninvasive magnetoencephalography (MEG) provide a millisecond portrayal of the neural dynamics underlying somatosensory processing and the gating of such...