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Hypertensive stress rewires macrophage signaling in heart failure with preserved ejection fraction independent of obesity

Pathological remodeling and functional evolution of the corneal nervous system in ocular surface dyshomeostasis

The corneal nerve plexus is essential to ocular surface homeostasis through sensory detection, trophic support, epithelial repair, blinking, and lacrimal reflexes. In dry eye disease (DED), chronic hyperosmolar, inflammatory, mechanical, and age-related stressors alter nerve morphology and function, contributing to reduced nerve density, aberrant regeneration, microneuroma formation, sensory loss, and peripheral or central sensitization. This review summarizes the ultrastructure of corneal innervation and the molecular basis of corneal sensory transduction, with emphasis on TRPM8, TRPV1, TRPA1, Piezo2, and acid-sensing ion channels. It then examines bidirectional neuroimmune signaling involving dendritic cells, cytokines, neuropeptides, and diminished neurotrophic support. We further discuss the relationship between age-related corneal hypoesthesia, local small-fiber degeneration, and sy

A History of Research into Cellular Senescence

Cells become senescent in response to various forms of damage and stress, including the stress induced by reaching the Hayflick limit on replication. This was first described in the context of replicative senescence in cell cultures, and from there cellular senescence became a topic of interest in cancer research. In more recent years, the accumulation of senescent cells in aged tissues was demonstrated to be an important contribution to degenerative aging, and a small industry of biotech companies has emerged to develop a variety of therapies to either selectively destroy or modulate the behavior of senescent cells. The history of cellular senescence is, in many ways, a history of expanding biological complexity. What began as an observation of finite proliferative capacity in cultured cells has […]

Age-Related Decline in Chaperone-Mediated Autophagy Impairs Clearance of Senescence Cells

Cells become senescent in response to stress and damage, in response to tissue injury, but most commonly upon reaching the Hayflick limit to replication. A senescent cell ceases to replicate, grows in size, and generates a potent mix of pro-growth, pro-inflammatory signals. Senescent cells are created throughout life in tissues throughout the body, but an established population of lingering senescent cells only begins to accumulate in later life. In youth, the immune system efficiently clears senescent cells, allowing senescence to be a beneficial state in the coordination of regeneration and in drawing the attention of the immune system to potentially cancerous cells. In later life, the immune system falters in this task. An established population of senescent cells that generates signaling constantly, even in relatively […]

Inflammatory and cardiac-stress biomarkers in Moyamoya disease: the role of GDF-15

BackgroundMoyamoya disease (MMD) is an uncommon cerebrovascular condition that requires the identification of easily measurable biomarkers to enable prompt diagnosis. This study aimed to: (1) compare clinical and laboratory parameters between individuals with MMD and control subjects; (2) examine the associations of these parameters with growth differentiation factor-15 (GDF-15); (3) evaluate the diagnostic effectiveness of potential biomarkers; and (4) identify independent risk factors for MMD.MethodsThe study cohort comprised 265 participants, including 121 patients diagnosed with MMD and 144 healthy control subjects. The parameters measured included white blood cell count (WBC), neutrophil count (NEU), Glu, homocysteine (HCY), GDF-15, and soluble growth stimulation expressed gene 2 (ST-2) concentrations. The analyses conducted encompassed correlation assessments, receiver operating ch

‘I want to do everything I can to head off dementia’: why demand for the shingles vaccine is soaring

Could a drug intended to prevent painful rashes also protect our brains as we get older? The signs are promising – but not conclusive. Yet that’s enough to be driving a boom in shingles jabs When Jenny, a 50-year-old marketing and branding professional from Cambridge, went for her shingles vaccine last year, an entirely different disease was on her mind. Having witnessed three of her four grandparents succumb to dementia, with all the distress that brought, she wants to avoid the same fate. She hopes the shingles vaccine might help. Jenny is far from alone. Britain’s high street chemists have reported a rise in demand for the shingles vaccine, at least some of which is driven by people more worried about dementia than shingles. And while the vaccine is free for some on the NHS, most under-65s pay around £450 for the full two doses. Continue reading...

Scientists discover 5 hidden brain patterns behind depression

Depression may not be one biological condition, but several distinct patterns of brain activity hiding under the same diagnosis. Researchers studying 263 people with depression identified five brain profiles, each showing different patterns of communication between brain regions and associations with symptoms such as anxiety, trauma, and substance abuse.

Direct Pharmacological Activation of AMPK Modestly Extends Life in Short-Lived Species

AMPK is the target of a range of interventions known to modestly slow aging in short-lived species. Like much of the complex array of evolved machinery that responds to various forms of cellular stress with improved maintenance, repair of damage, and a consequent slowing of aging, AMPK is involved in the regulation of energy metabolism. Many of these interventions, such as metformin, are far from robust. The animal data is mixed. One might argue that this is in part because the effects on the behavior of AMPK are indirect, as researchers do in this paper. Still, their direct approach to activating AMPK still produces only a modest effect on life span, and does so in species known to be far more receptive to life extension […]

The future of peptide medicine is about closing the gray market

As peptides surge in popularity, better evidence and cleaner supply chains could help the field grow without leaving patients behind. Peptides have become one of longevity’s biggest concepts. However, behind the social media posts and “research use only” vials is a more complicated reality: demand is moving faster than the systems designed to make these […] The post The future of peptide medicine is about closing the gray market appeared first on Longevity.Technology.

Exercise program supports better attention and slows biological aging in breast cancer survivors

One in three breast cancer survivors will experience cognitive problems, which can include difficulties with attention, memory, processing speed and other aspects of thinking. Researchers believe these problems can arise from a combination of treatment effects, inflammation, hormonal changes, fatigue and stress. They may persist after treatment and affect everyday activities and quality of life.

Selective autophagy inhibition alleviates oxidative stress-associated neurodegeneration in an AD+CCH model

Dysregulated autophagy is increasingly implicated in the progression of Alzheimer's disease (AD), particularly when chronic cerebral hypoperfusion (CCH) coexists and exacerbates neurodegeneration. However, the relationship between autophagy dysregulation and oxidative stress responses under combined AD+CCH conditions remains incompletely understood. Here, APP/PS1 transgenic mice subjected to CCH were used to evaluate the effects of autophagy modulation with 3-methyladenine (3MA) and rapamycin (RAPA). CCH worsened cognitive impairment and neuronal injury in APP/PS1 mice and was accompanied by altered LC3-II and p62 expression, consistent with disturbed autophagy-related processing. These changes occurred together with increased expression of proteins associated with oxidative stress responses, including Keap1, Nrf2, HO-1, HIF-1α, and NOX-1. Notably, 3MA improved behavioral performance, re

Self-reported chewing or swallowing problems and episodic memory performance in older Americans: a longitudinal cohort study

BackgroundImpaired mastication is a plausible modifiable risk factor for dementia, but long-term longitudinal evidence using functional metrics instead of tooth counts is limited. This study investigated the association between self-reported chewing/swallowing problems and cognitive decline trajectories in older adults.MethodsWe analyzed repeated NHATS rounds 7–14. The primary analytic sample comprised 8,636 participants contributing 34,571 person-round observations with valid exposure and immediate plus delayed 10-word recall. Raw total recall (0–20) was the primary outcome. Linear mixed models used rounds since each participant’s first complete analytic assessment, time-varying exposure, random intercepts and random slopes, and adjustment for age, sex, race/ethnicity, education, comorbidity count, depressive symptoms, hearing impairment, and vision impairment.ResultsAt the first comple

Britons are not ageing healthily – we need to learn from countries that have made it a priority | Devi Sridhar

Although we’re living longer, the data on healthy life expectancy in the UK isn’t good. Andy Burnham must reverse this trend to protect the NHS and social care Prof Devi Sridhar is chair of global public health at the University of Edinburgh, and the author of How Not to Die (Too Soon) The prime minister has put forward his bold proposal for a universal, NHS-style social care service. In doing so, Andy Burnham has put the spotlight back on one of the major challenges facing almost everywhere in the world: how to manage the demographic changes linked to an ageing society. It’s an important discussion. But what if government didn’t just look at how to care for people in their later years and instead spent real political capital on policies to help people live longer independently, and in good health? The data isn’t pretty on this. While the trend over the past half-century in almost all co

Dysfunction of lipid metabolism and lysosomal capacity: at the core of microglial aging?

As primary immune cells of the central nervous system (CNS), microglia maintain immune surveillance, inflammation regulation, cell interactions and debris clearance. These dynamic and adaptive effector functions are reciprocally sustained by microglial metabolism. Lipids are emerging as a key programmer of microglial metabolic and functional flexibility in conditions of homeostasis, cellular stress, and pathology. The delicate equilibrium in microglial lipid homeostasis is dependent on the integrated activity of all cellular components, including the lysosome-lipophagy pathway. Continuous adaptations in microglial metabolism contribute to a cumulative imbalance between lysosomal network capacity and the efficacy of lipid turnover in aged microglia. The disequilibrium contributes to microglial fatigue and detrimental homeostatic activity associated with aging. Lipid droplet-accumulating m

Scientists gave worms magnetic bacteria. They lived 43% longer

A magnet-producing bacterium extended the average lifespan of C. elegans worms by more than 43% while helping protect their neurological and intestinal health. Researchers traced much of the effect to suppression of ferroptosis, a damaging form of cell death linked to iron buildup and oxidative stress.

Mediating effect of social frailty on oral frailty and cognitive function in older adults: a cross-sectional study in a rural Chinese community

BackgroundCognitive function has been associated with both social and oral frailty. However, few studies have explored how social frailty and oral frailty jointly relate to cognitive function. This study aimed to explore whether social frailty plays a mediating role in the association between oral frailty and cognitive function and to examine potential gender differences in this pathway.MethodsThis was a cross-sectional study design, and the data were obtained from the 2022 follow-up survey of the Health Status of Rural Older Adults (HSRO). The Mini-Mental State Examination (MMSE) was used to assess cognitive function, the Tanaka’s Oral Frailty Index-8 (OFI-8) was used to assess the risk of oral frailty, and social frailty was assessed using an operational definition that included five items: going out less frequently, rarely visiting friends, feeling unhelpful to friends or family, livi

Gut-brain immune dysregulation in Parkinson’s disease: a hypothesis-forming narrative review of trained immunity

Parkinson’s disease (PD) is increasingly understood as a multisystem disorder in which gastrointestinal dysfunction, immune remodeling, protein aggregation, and central neurodegeneration interact across the disease course. Although gut microbiota alterations are repeatedly reported in PD, taxonomic differences alone do not explain how peripheral ecological signals acquire neurological relevance. This review therefore focuses on immune translation: the processes through which dysbiosis, microbial metabolites, intestinal barrier stress, and mucosal inflammation may reshape peripheral immunity and lower the threshold for central neuroinflammatory responses. Particular attention is given to trained immunity as a mechanistic framework that may connect repeated low-grade gut-derived stimulation with persistent innate immune reprogramming. Direct evidence that trained immunity drives PD remains

Peroxisomes in Alzheimer’s disease: emerging mechanistic insights and therapeutic opportunities

Alzheimer’s disease (AD) is characterized by amyloid-β (Aβ) deposition, tau pathology, synaptic injury, neuroinflammation, oxidative stress, and disrupted organellar homeostasis. Peroxisomes maintain lipid and redox balance through very-long-chain fatty acid (VLCFA) β-oxidation, plasmalogen biosynthesis, and reactive oxygen species (ROS) metabolism. This Review evaluates how peroxisomal alterations may modulate APP processing and Aβ clearance, tau kinase/phosphatase balance, neuroinflammation, oxidative stress, and peroxisome-mitochondria crosstalk. We distinguish human correlational evidence from intervention studies in AD models and mechanistic extrapolation from primary peroxisomal disorders. Current evidence supports a context-dependent vulnerability or amplifier model rather than a universal causal pathway. Peroxisome-targeted interventions remain investigational, and no validated b

Neuropeptide Y and brain ageing: an updated scoping review on the role of autophagy

Brain ageing is a complex physiological process characterised by progressive structural and functional changes that often result in cognitive decline and reduced quality of life in the elderly. These changes are driven by multiple mechanisms, including synaptic dysfunction, oxidative stress, neuroinflammation, and impaired cellular homeostasis. Neuropeptides have emerged as important regulators of these processes. Among them, neuropeptide Y (NPY) has gained attention for its potential role in mitigating age-related brain dysfunction. However, the extent to which NPY contributes to brain ageing remains unclear. This scoping review aims to map the available evidence on the role of NPY in brain ageing, focusing on the effect of NPY on autophagy, a key mechanism involved in brain ageing. Scientific studies published between 2014 and 2026 relevant to the research topic were systematically scr

Telomir-Zn restores vision and repairs eye damage in age-related study

A peer-reviewed paper published in the International Journal of Molecular Sciences reports that Telomir-Zn significantly improved visual function, restored thickness across multiple retinal layers and reduced mitochondrial oxidative stress in a zebrafish model of mitochondrial dysfunction and age-related retinal degeneration. Telomir Pharmaceuticals claims treatment produced dose-dependent increases in relative telomeric DNA content and restoration of […] The post Telomir-Zn restores vision and repairs eye damage in age-related study appeared first on Longevity.Technology.

Oxidation of SOD1 in Skin Aging

Normal cell metabolism, particularly the activities of mitochondria, generates oxidizing molecules that react with proteins to disrupt their function. This damage occurs constantly, and is repaired constantly. Cells remove damaged proteins, undo oxidative changes, and make use of antioxidant enzymes such as SOD1 to prevent damage from occurring in the first place. With age, oxidation increases and becomes an important component of cell dysfunction. Here, researchers note that SOD1 itself can become oxidized and harmful, and discuss the importance of antioxidants disabled by oxidization in the growth of age-related oxidative stress in cells. The specific focus is on skin aging, but the points have relevance to all tissues. As the body's primary barrier against environmental insults, the skin is continually exposed to oxidative stress, which […]

Researchers warn social media driving harmful misuse of Alzheimer’s blood tests

Exclusive: Screening if used alone risks leading people to believe they are inevitably going to develop dementia Follow our Australia news live blog for latest updates Get our breaking news email, free app or daily news podcast Researchers have warned that social media may be misleading healthy people into taking Alzheimer’s blood tests, causing severe anxiety over biological markers that may never actually cause dementia. Blood-based biomarker tests, including p-tau217 and p-tau181, detect biological signs of changes in the brain associated with Alzheimer’s disease, which is a progressive brain disorder and the leading cause of dementia. Continue reading...

P2RX7 Antagonism Reduces Macrophage Senescence in the Aging Kidney

Cells become senescent constantly throughout life in response to various forms of damage and stress, ceasing replication and generating a potent mix of inflammatory signals. In youth, these cells are promptly cleared by the immune system, but with advancing age they begin to linger and accumulate. The inflammatory signaling becomes disruptive to tissue structure and function when sustained over the long term, and this is an important contribution to degenerative aging. Here, researchers show that macrophage cells in the kidney express increasing amounts of the P2RX7 receptor on the cell surface as they progress towards becoming senescent, and blocking this receptor with a suitable antagonist small molecule reduces macrophage senescence and improves kidney function. Macrophage senescence is a pathological feature in aging or diseased kidneys. […]

I’m a psychoanalyst. Social media is damaging children’s inner lives in ways we don’t fully understand | Robin Kirman

Discussion has focused on behavioral outcomes. But Meta’s settlement shines a light on damage to young people’s emerging desires and identities During the landmark social media addiction trial that led to Meta’s recent $17.1bn settlement, a therapist testified that she had once asked the plaintiff – a young woman named Kaley, who had been using social media since she was six – what her miracle day would look like: what she wished to come true, if anything were possible. Kaley replied that she would be prettier. As a psychoanalyst, I find that exchange devastating in a particular way. A miracle day is an invitation to engage with the full range of human desire: with what one might accomplish or experience, whom one might encounter or love. Kaley’s answer contracted the world and all its possibility into a single preoccupation with her own image. Continue reading...

Inflammation Driven by Fat Cells as a Contribution to Atherosclerosis

Atherosclerosis is the largest cause of human mortality, producing stroke and heart attack when fatty plaques obstructing arteries rupture. There is accordingly a great deal of research aimed at influencing the course of the condition. Reversal of plaque growth to clear arteries and remove potentially unstable plaques remains a challenge, and few approaches have been shown to achieve this goal with any reliability even in animal studies. Conversely, many different approaches have been shown to slow the development of atherosclerosis in high fat diet mouse models of the condition. The example here is a demonstration of the degree to which maladaptive fat tissue metabolism contributes to the environment of inflammation and cell stress that accelerates the growth of atherosclerotic plaque. Unfortunately, like so many other […]

Comprehensive analysis of circRNA-miRNA-mRNA networks to reveal potential cell death, inflammation and oxidative stress-related targets for postoperative cognitive dysfunction

BackgroundPostoperative cognitive dysfunction (POCD) is a common neurological complication involving the hippocampus, a brain region critical for learning and memory. Circular RNA (circRNA) plays an important role in regulating gene expression. Our objective is to predict and verify a circRNA-miRNA-mRNA network in POCD.MethodsMicroarray data of POCD mouse models were retrieved from the Gene Expression Omnibus (GEO) database. Differential expression analysis was used to identify differentially expressed circRNA, miRNA, and mRNA. An in silico circRNA-miRNA-mRNA network was subsequently predicted based on miRNA-mRNA pairs and miRNA-circRNA pairs obtained from public databases. From this global network, three hub subnetworks based on the competing endogenous RNA (ceRNA) hypothesis were analyzed. In hippocampal tissue of POCD mice, RT-qPCR quantified key circRNAs, miRNAs, and mRNAs, with prot

Forget memory tests: Could sleep catch Alzheimer’s first?

Researchers say disrupted sleep may be one of the earliest signs of Alzheimer’s, arriving years before memory loss and reshaping drug trials. Most people chalk up a bad night’s sleep to stress, or to simply getting older. A growing body of research suggests something less comfortable: in some cases, disrupted sleep isn’t just an inconvenience […] The post Forget memory tests: Could sleep catch Alzheimer’s first? appeared first on Longevity.Technology.

Automation of Screening Studies for Compounds that Slow Aging is Becoming More Ambitious

Screening compound libraries for effects on aging in short-lived species has grown to become a significant area of interest in the aging research community. As a general rule, discoveries are modest in effect size, and largely take the form of novel ways to influence the beneficial maintenance and repair activities (such as autophagy) triggered by calorie restriction, heat, cold, and other forms of stress. These responses have a much larger effect on life span in short-lived species than in long-lived species, so in the long run are not all that interesting. Nonetheless, considerable effort has been made to find ways to make this screening process more efficient and automated. Research equipment has been constructed to house tens of thousands of nematode worms and use machine […]

Brain metabolic and network profiles characterized by comorbid depressive symptoms and sleep disturbances in Parkinson’s disease: an 18F-FDG PET study

BackgroundParkinson’s disease (PD) is a globally increasing neurodegenerative disorder. Its complex, multisystem pathophysiology extends beyond dopaminergic neuron loss and gives rise to diverse clinical manifestations. This exploratory study examined brain metabolic patterns in patients with PD and depressive symptoms (PD-Dep) or sleep disturbances (PD-SD).MethodsTwenty-eight patients with PD assessed between December 2019 and January 2024 were included. Sixteen met the HAMD threshold for PD-Dep, 21 met the PSQI threshold for PD-SD, and nine met both criteria; the cohorts were therefore overlapping symptom-defined groups. Seventeen healthy participants served as controls (HC). All participants underwent 18F-FDG PET. Voxel-wise group contrasts and exploratory AAL-based partial correlations with HAMD, PSQI, and UPDRS-III were examined.ResultsAt the prespecified liberal voxel-wise cluster-

CRISPR-based functional genomic screening in neurodegeneration: mechanistic insights into AD, PD, and ALS

Neurodegenerative diseases, including Alzheimer's disease (AD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS), are characterized by pronounced clinical and molecular heterogeneity, as well as highly interconnected pathogenic pathways. This biological complexity has long hindered efforts to systematically define disease mechanisms and to develop effective, targeted therapies. In recent years, clustered regularly interspaced short palindromic repeats (CRISPR) based functional genomic screening technologies have emerged as powerful tools for large-scale genetic perturbation in cellular, organoid, and in vivo models, enabling unbiased interrogation of disease relevant genetic networks and the identification of potential therapeutic targets. In this review, we summarize CRISPR knockout, CRISPR interference, CRISPR activation, and in vivo screening studies in AD, PD, and AL

Sensory impairment and cognitive-state transitions in middle-aged and older adults: a multistate Markov analysis of the health and retirement study

BackgroundSensory impairment has been associated with cognitive decline and dementia. However, endpoint-based longitudinal analyses often cannot determine whether sensory impairment is related to early cognitive deterioration, reduced cognitive recovery, dementia progression, or mortality-related study exit.MethodsWe analyzed 2004–2022 Health and Retirement Study data using a continuous-time multistate Markov model. Four states were defined: normal cognition, cognitive impairment no dementia (CIND), dementia, and death. The analytic cohort included 18,292 participants, and 16,083 were included in the primary complete-case adjusted model. Baseline self-reported sensory status was classified as no impairment, visual impairment only, hearing impairment only, or dual sensory impairment. Primary models adjusted for age, sex, education, wealth, depressive symptoms, and chronic disease count; s

Early mitochondrial stress reveals potential mechanism for lasting heart protection

Mitochondria are popularly known as the "powerhouse of the cell," but these cellular structures do much more—including acting as signaling hubs. Some signals that mitochondria send can reprogram the activity of the entire cell by switching "on" or "off" different genes through epigenetic changes. Mitochondria's signals can be so effective that, in yeast, fruit flies and worms, mild stress in mitochondria early in life can make the entire organism more resilient and live longer through a process called mitohormesis.

Senescent Microglia Secrete DLK1, Which Causes Dysfunction in the Aging Brain

Senescent cells accumulate with age in tissues throughout the body, disrupting tissue structure and function with inflammatory secretions. The growing burden of senescent cells is an important contributing cause of degenerative aging. A cell becomes senescent in response to damage induced by some form of stress, or more often when a somatic cell reaches the Hayflick limit on cellular replication. In youth senescent cells are efficiently cleared by the immune system, but immune system aging allows senescent cells to linger and grow in number. Immune cells themselves are prone to reaching the Hayflick limit and entering replicative senescence because they respond to a variety of issues with greater replication to multiply their efforts. Research into neurodegenerative conditions and the state of the aging brain has […]

Ferroptosis–neuroinflammation interplay: mechanistic pathways and therapeutic opportunities in central nervous system disorders

Oxidative stress, iron dyshomeostasis, and chronic neuroinflammation are the principal mechanisms involved in the progression of central nervous system (CNS) disorders, which are a significant source of death and chronic disability worldwide. This review focuses on understanding the mechanistic relationship between ferroptosis and neuroinflammation in central nervous system (CNS) disorders, which involves the molecular mechanisms, their role in the pathogenesis of the disease, and therapeutic opportunities available. Ferroptosis is a regulated form of cell death triggered by iron-catalyzed lipid peroxidation, glutathione depletion and inactivation of glutathione peroxidase 4 (GPX4), resulting in neuronal injury. The increased generation of ROS in the cell due to the presence of excess iron catalyzes Fenton chemistry, which leads to lipid peroxidation of the cell membrane and ferroptotic

Engram cell vulnerability in neurodegeneration: from mechanistic insights to therapeutic horizons

Neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD), and Huntington’s disease (HD) share progressive memory impairment, yet their upstream pathologies differ. This review synthesizes evidence across these disorders to frame memory decline through engram ensembles and proposes an excitability-vulnerability tradeoff, in which the physiological requirements for engram function, including elevated excitability, synaptic plasticity, and coordinated network activity, also increase sensitivity to synaptic stress, network disruption, and inflammatory perturbations. We summarize disease-related pathological cascades. To date, AD has the most robust body of direct experimental evidence linking pathology to impaired engram function. Solid experimental findings demonstrate that amyloid-β (Aβ)/tau causes hippocampal engram inaccessibility in AD. For PD and HD, infere

Joint network analysis of non-motor symptoms and quality of life in patients with Parkinson’s disease

BackgroundNon-motor symptoms (NMS) are highly prevalent in Parkinson’s disease (PD) and are major determinants of declining quality of life (QoL), yet traditional statistical approaches are insufficient to capture the complex interactions between NMS and QoL. Network analysis offers a promising alternative for exploring these interactions.ObjectiveTo construct a joint network of non-motor symptoms (NMS) and quality of life (QoL) in patients with Parkinson’s disease (PD), identify core and bridge nodes, and inform precision nursing interventions.MethodsA convenience sample of 342 PD patients was recruited between January and June 2026 from the PD specialty outpatient clinic and neurology inpatient wards of a tertiary specialized hospital in Tianjin, and investigated using the Non-Motor Symptoms Scale (NMSS) and the Parkinson’s Disease Questionnaire-39 (PDQ-39). A joint network model was c

Advances in the treatment of age-related hearing loss: from molecular mechanisms to targeted interventions

Age-related hearing loss (ARHL) is the most common sensory disorder in older adults. Current hearing interventions, including hearing aids and cochlear implants, face limitations in accessibility and adherence. Therefore, efforts have been devoted to elucidating the molecular mechanisms underlying cochlear aging and identifying effective therapeutic targets for ARHL. This review summarizes several molecular mechanisms implicated in cochlear aging and ARHL, including autophagy dysregulation, oxidative stress, stereocilia degeneration, and dysregulation of mitochondrial dynamics. We further discuss recent advances in potential therapeutic targets and intervention strategies associated with these pathways, and provide theoretical support for targeted interventions for ARHL.

Inflammation and neuropsychiatric symptoms in Parkinson's disease: a genetic association

BackgroundThere has been some evidence that neuroinflammation is involved in Parkinson's disease (PD) and in psychiatric disorders.ObjectiveTo explore the effects of IL-1β rs16944 on PD patients' neuropsychiatric symptoms.MethodsTwo hundred and eighty-one consecutive PD patients underwent a neurological and neuropsychological evaluations, which included: Unified Parkinson's Disease Rating Scale, Schwab and England Activities of Daily Living scale, Questionnaire for Impulsive-Compulsive Disorders in Parkinson's Disease—Anytime Short, Hospital Anxiety and Depression Scale and Dementia Rating Scale-2. The Neuropsychiatric Inventory (NPI) was also applied to patients' caregivers/informants. In addition to IL-1β rs16944, DRD3 rs6280 and GRIN2B rs7301328 were also genotyped. Non-parametric group comparisons and linear and logistic regressions were used for data analyses.ResultsThe IL-1β rs1694

Dogs may hold surprising clues to human longevity

Dogs and humans may have more in common when it comes to aging than scientists realized. Researchers with the Dog Aging Project found that patterns of small molecules in dogs’ blood were linked to longer or shorter lifespans in remarkably similar ways to those seen in people. These metabolic “fingerprints” could offer clues about the biological processes that drive aging, including metabolism, inflammation, and cellular stress.

In ALS, Microglia Eat Living Neurons, Mistaking Them for Dead

A new study suggests that in amyotrophic lateral sclerosis – and possibly other neurodegenerative diseases – the brain’s immune cells devour stressed but still […]