Mental and Cognitive Health Library
Every article, presentation, spotlight, and news item we've tagged to Mental and Cognitive Health.
Showing 121–144 of 203
Quantitative brain imaging detects MS decline before symptoms emerge
Viz.ai and Cortechs.ai are integrating quantitative brain imaging into clinical workflows to detect neurological decline through objective measurement rather than visual comparison. This partnership represents a shift from subjective radiologist interpretation to measurable biomarkers in multiple sclerosis care, with implications for earlier intervention in neurodegenerative disease.
CB2 Activation Reduces Neuroinflammation in Alzheimer's Phase 2a
NeuroTherapia's Phase 2a trial of NTRX-07 in mild cognitive impairment and mild-to-moderate Alzheimer's disease showed reduced neuroinflammation on MRI and stabilized neurofilament light chain in cerebrospinal fluid, with favorable safety and tolerability. These findings suggest CB2 receptor activation may modulate the neuroinflammatory and amyloid pathology underlying cognitive decline.
ALS drug PrimeC cuts death risk by 65%
Long-term follow-up data from NeuroSense's PrimeC trial in ALS patients demonstrates a 65% reduction in death risk and median survival extension of 14+ months—a magnitude rarely achieved in neurodegenerative disease. This represents a potential shift from symptomatic management toward disease modification in a rapidly progressive condition.
#382 ‒ AMA #80: Longevity optimization through strength benchmarks, VO₂ max targets, nutrition principles, brain health, supplements, GLP-1 RAs, wearables, and more
Exercise emerges as the most protective intervention for brain health across the lifespan, with specific performance benchmarks in strength and aerobic capacity serving as measurable proxies for cognitive preservation and longevity. This positions physical capacity as a foundational biomarker that integrates multiple physiological systems rather than a secondary health outcome.
GLP-1 drugs fail to slow cognitive decline in Alzheimer’s disease
Recent evidence indicates GLP-1 receptor agonists do not slow cognitive decline in established Alzheimer's disease, despite theoretical mechanistic rationale and their known metabolic benefits. This finding redirects focus toward earlier intervention windows and prevention strategies rather than disease reversal in advanced stages.
Human brain aging decoded through living tissue
Researchers mapped how living human brain cells coordinate structural changes across the lifespan, revealing that brain aging is an active, regulated biological process rather than passive deterioration. This represents the first large-scale analysis of living tissue, enabling identification of molecular targets for intervention in age-related neurological decline.
Microglial Metabolism Drives Cognitive Aging
Microglia—the brain's immune cells—undergo metabolic shifts with age that correlate with chronic inflammation and increased risk of neurodegenerative disease. These metabolic changes are reversible targets for intervention, offering a mechanistic pathway to slow cognitive decline and protect against Alzheimer's and Parkinson's disease.
The dynamic physiology of the brain with menopause
Brain imaging reveals menopause involves significant neurological changes beyond reproductive shifts, with alterations in cerebral blood flow, neural connectivity, and metabolic function that persist into the post-menopausal years. Understanding these changes is essential for optimizing cognitive function and preventing age-related neurological decline in midlife women.
Neuron-specific mitophagy decline reveals aging's uneven cognitive impact
Selective removal of damaged mitochondria varies by neuron type in aging brains, with certain cells losing mitophagy capacity earlier than others. This cell-specific decline in mitochondrial quality control directly impacts neural energy metabolism and may explain differential cognitive aging patterns across brain regions.
Epigenetic Clocks of Biological Aging and Risk of Incident Mild Cognitive Impairment and Dementia: The Women's Health Initiative Memory Study
Accelerated biological aging measured by the epigenetic clock AgeAccelGrim2 was associated with increased risk of mild cognitive impairment and dementia in 6,069 cognitively unimpaired women over 9.3 years of follow-up, independent of chronological age. This establishes epigenetic markers as measurable indicators of neurodegeneration risk.
Digital cognition testing closes early detection gap in Alzheimer's
Plasma biomarkers can identify Alzheimer's pathology years before cognitive decline becomes clinically apparent, yet clinical assessment protocols lag far behind this detection capability. Digitized cognitive testing that targets vulnerable neural networks bridges this gap, enabling functional decline detection concurrent with biomarker identification—a prerequisite for meaningful early intervention.
APOE variants shape brain protein patterns before neurodegeneration
APOE ε2 and ε4 genetic variants produce distinct proteomic signatures that emerge before amyloid accumulation, mechanistically explaining their opposing effects on Alzheimer's disease risk. This proteomic mapping offers a foundation for identifying intervention points specific to genetic risk profiles rather than treating all cognitive decline uniformly.
Pathways to Falls Among Community-Dwelling Older Women: The Mediating Role of Cognitive Decline and Fear of Falling
Fear of falling and cognitive decline act as mediating pathways linking physical and psychological risk factors to fall incidence in older women living in community settings. This identifies actionable intervention points beyond treating isolated fall risk factors.
Infection-Triggered Neuroinflammation Links Acute Illness to Dementia
Severe infections predict subsequent dementia risk independent of frailty or comorbidity burden, suggesting infection-related neuroinflammation may trigger lasting cognitive decline. This connection identifies a modifiable pathway in dementia prevention that operates through acute immune activation rather than baseline health status alone.
Social isolation accelerates molecular aging via epigenetic pathways
Social experiences correlate with mortality risk through measurable physiological pathways: epigenetic aging, allostatic load, and health status. This evidence demonstrates that the quality and frequency of social engagement directly influence aging rate and disease burden at the molecular level.
Glycosylation Dysregulation Drives Alzheimer's Neurodegeneration
Hyperglycosylation—excessive attachment of complex carbohydrates to proteins—emerges as a hallmark molecular feature of Alzheimer's disease, concentrated in memory and cognitive regions. Experimental reduction of glycosylation improved behavioral outcomes in animal models, suggesting this metabolic alteration may be a causal driver rather than merely a downstream consequence.
Isolation Triggers Inflammatory Oxylipin Surge in Aging
Social isolation in aged mice triggers a substantial increase in lipoxygenase-derived oxylipins, pro-inflammatory lipid mediators that amplify systemic inflammation. This finding establishes a direct biochemical pathway linking psychological stress to accelerated aging through altered lipid metabolism and immune dysregulation.
PREMAZ expands early brain screening through Health is One
PREMAZ, a digital cognitive assessment tool, has partnered with Health is One to integrate early brain screening into everyday wellness services rather than clinical settings. The platform measures memory precision—the sharpness and reliability of recall—to detect subtle cognitive changes before decline becomes clinically apparent, shifting brain health assessment from reactive to preventive.
Menopause timing predicts brain metabolic decline
Early menopause correlates with measurably reduced whole-brain metabolic activity, suggesting estrogen's role in maintaining cerebral energy production extends beyond reproductive function. This finding connects reproductive aging to neurological reserve and cognitive longevity.
Sleep rhythms and dementia risk link emerges
Chronic circadian disruption triggers structural changes in microglia, shifting them toward an inflammatory, stress-primed state that impairs their ability to clear neural debris. This mechanism may represent a primary driver of brain aging and dementia risk decades before cognitive symptoms emerge, with emerging research exploring whether stem cell-derived extracellular vesicles can intercept this inflammatory cascade.
Mitochondrial RNA Dysfunction Drives Brain Aging Inflammation
Mitochondrial double-stranded RNA accumulates in the brain after midlife, with levels further elevated in Alzheimer's disease where they correlate with cognitive decline. This accumulation reflects disrupted RNA processing machinery and triggers chronic inflammatory signaling, establishing mitochondrial RNA homeostasis as a measurable driver of age-related neurodegeneration.
Air Quality Gains Fade Against Population Aging in Dementia
Population aging in China is driving dementia mortality increases that outpace the protective effects of air quality improvements. Without substantially more aggressive pollution control, aging demographics will continue to erode the cognitive health gains achieved through reduced particulate matter exposure.
New findings link autophagy failure to early Alzheimer’s pathology
Impaired neuronal autophagy precedes amyloid-beta and tau pathology in Alzheimer's disease, suggesting that restoring cellular clearance mechanisms may address disease onset at a mechanistic level upstream of classical biomarkers. This positions autophagy dysfunction as a tractable target for intervention before irreversible neurodegeneration.
Psilocybin and human longevity
Psilocybin demonstrates measurable effects on lifespan and healthspan markers in preclinical models, operating through neuroplasticity pathways and stress-response modulation. The compound's capacity to alter consciousness-linked neural signaling raises questions about its role in longevity pathways previously associated with psychological resilience and systemic stress tolerance.