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At least 19 recordsLinked to original sources
PubMed2025

Brain Health Loss Mediates the Effect of Infarct Volume on Functional Outcome in Ischemic Stroke.

IMPORTANCE: Brain health may facilitate resilience to detrimental consequences from neurological diseases. Infarct volume is associated with poor functional outcome after acute ischemic stroke (AIS), but potential mediating effects through stroke-related brain health loss have not been investigated. OBJECTIVE: To determine whether stroke-related brain health loss, quantified by change in MRI derived effective Reserve (eR), mediates the effect of acute infarct volume on functional outcome after AIS. DESIGN: Observational multicenter cohort study. SETTING: We analyzed data from the GASROS (n=488) and MRI-GENIE (n=560) cohorts, collected 2003-2011. PARTICIPANTS: Adult patients consecutively diagnosed with AIS, with available admission MRI. EXPOSURE: At admission, white matter hyperintensity (WMH) and normal-appearing brain volumes were assessed on T2-FLAIR, and acute infarct volume on diffusion weighted imaging. WMH was normalized by brain volume, creating WMH load. We quantified brain health using eR, a latent variable incorporating age, WMH load, and normal-appearing brain volume. &#x394;eR reflected the change in eR when acute infarct volume was included, representing stroke-related brain health decline. Mediation analysis was used to determine if &#x394;eR mediates the effect of infarct volume on functional outcome (modified Rankin Scale [mRS] at 90 days). MAIN OUTCOME MEASURE: Proportion of mediating effect. RESULTS: We included 1,048 patients (median age 67y, 38% females). At baseline, median NIHSS score was 3 (IQR 1-7), median infarct volume 3.1mL (IQR 0.9-15.5). At 90 days, median mRS score was 1 (IQR 1-3) and 51 (5%) patients had died. In mediation analysis, &#x394;eR significantly mediated 36% (95% CI 16-56%) of the total effect of infarct volume on functional outcome (direct effect (&#xdf;=0.15 [95% CI 0.09-0.22], p<0.001; indirect effect mediated through &#x394;eR: &#xdf;=0.09 [95% CI 0.04 to 0.14], p=0.001). In subgroup-analyses, the mediative effect was apparent among female but not male, and among patients aged >67y but not &#x2264;67y. CONCLUSIONS AND RELEVANCE: Stroke-related structural brain health loss mediates about one third of the effect of acute infarct volume on functional outcome after ischemic stroke, with important sex and age differences. Brain health significantly influences outcome and recovery potential, and may be considered a key biomarker when modeling outcome after AIS.

acute ischemic stroke↗
PubMed2025

Associations Between Walking Pace, APOE-&#x3b5;4 Genotype, and Brain Health in Middle-Aged to Older Adults.

PURPOSE: This study aimed to investigate whether self-reported walking pace (a marker of physical function) and the presence of APOE-&#x3b5;4 allele interact to modify brain health outcomes. METHODS: We used data from a prospective cohort study of middle-aged to older adults from the UK Biobank who self-reported walking pace (slow or steady-to-brisk) and who were initially free of dementia ( n = 415,110). Incident all-cause dementia was obtained from hospital and death registry records, and structural brain volumes (right and left hippocampus volumes, total gray matter volume, and volume of white matter hyperintensities) were measured from a subset of participants ( n = 33,113). Cox proportional hazard models and generalized linear models were used to assess associations between exposures and outcomes. RESULTS: Slow walking pace and the presence of APOE-&#x3b5;4 allele were associated with increased dementia risk (HR = 1.79 [95% CI = 1.66-1.93], P < 0.001; HR = 3.06 [2.90-3.23], P < 0.001, respectively), and there was an interaction between these associations, indicating that the association of walking pace with dementia risk is modified by APOE-&#x3b5;4 status (reference group: HR Steady-Brisk/APOE-&#x3b5;4- = 1; HR Slow/APOE-&#x3b5;4- = 2.03 [1.84-2.25], P < 0.001; HR Steady-Brisk/APOE-&#x3b5;4+ = 3.21 [3.02-3.41], P < 0.001; HR Slow/APOE-&#x3b5;4+ = 4.99 [4.48-5.58], P < 0.001). Slow self-reported walking pace was associated with worse brain volume outcomes, and these associations were not modified by APOE-&#x3b5;4 genotype. CONCLUSIONS: These results suggest walking pace and APOE-&#x3b5;4 status independently influence brain volume outcomes, but both factors independently and jointly contribute to increased dementia risk. Individuals with both risk factors (slow walking pace and APOE-&#x3b5;4 allele) show the strongest associations with dementia risk.

Self Report↗
PubMed2026

One brain, one mind: A joint EPA-EAN leadership perspective on brain health.

Neurology and psychiatry have operated as separate disciplines for over a century, yet this division reflects historical and institutional developments rather than the underlying biology of the brain. Contemporary neuroscience shows that brain and mental health disorders share genetic susceptibilities, inflammatory and metabolic pathways, environmental and social risk factors, and clinical features that cross diagnostic boundaries. Cognitive, emotional, sensory, and motor symptoms regularly appear across both neurological and psychiatric populations, and conditions such as seizures, psychosis, mood disorders, cognitive disorders, and sleep disorders are common to both. A brain health framework addresses this reality by treating the brain as a single biological organ whose function emerges from the interplay between genome and exposome - including stress, trauma, social context, existential meaning, pollution, and physical health - and which underlies perception, behaviour, cognition, emotion, resilience, and vulnerability. Translating this perspective into practice requires coordinated action across domains. Clinically, collaborative models such as joint neurology-psychiatry consultations and shared outpatient pathways can be implemented within existing resources to improve diagnostic clarity and continuity of care. In training, a more harmonised curriculum with shared foundations in neurobiology, joint seminars, and cross-rotations would equip clinicians with a common language while preserving specialist depth, and support the emerging fields of preventive neurology and preventive psychiatry. In research, organising studies around shared mechanisms and symptom dimensions, and launching joint funding calls, would enhance translational relevance and reduce duplication. To realise this vision, sustained leadership from European professional bodies is essential to establish collaboration as a shared professional standard.

Humans↗
PubMed2006

Interactive effects of fitness and hormone treatment on brain health in postmenopausal women.

Recent research in rodents suggests that extended and chronic hormone therapy can exacerbate memory impairments and irreversibly damage cells. However, aerobic fitness regimens have been shown to spare brain tissue and cognitive function. In addition, interactions between estrogen treatment and exercise have been reported in rodents. However, whether aerobic fitness and hormone treatments show interactive effects on human brain tissue and cognition has yet to be determined. Here we report two unique and important results: (a) HRT treatment up to 10 years in duration spares gray matter in prefrontal cortex and is associated with better performance on measures of executive function, whereas HRT treatment beyond 10 years in duration increases the degree of prefrontal deterioration and amplifies the decline on measures of executive functioning (b) higher fitness levels augment the effects of shorter durations of hormone treatment and ameliorate the declines associated with prolonged hormone treatment.

Aged↗
PubMed1993

Age-related decline of psychomotor speed: effects of age, brain health, sex, and education.

A cross-sectional study into age-related decline of psychomotor speed is reported. A newly introduced choice response task was used, involving three conditions: simple reaction time (SRT), choice reaction time (CRT), and CRT with stimulus-response incompatibility. Subjects were 247 volunteers, aged 20 to 80 yr. in seven age levels. Although all subjects thought themselves to be normal and healthy, a post hoc division could be made based on biological life events (BLE, mild biological or environmental factors that can hamper optimal brain functioning, such as repeated general anesthesia). Performance was poorer by subjects who had experienced one or more such event: slowing was comparable to the effect of age, especially in the more difficult task conditions. There were significant effects of sex and education, men being consistently faster than women, and more highly educated subjects performing better than subjects with only low or medium education. These findings replicate observations from other test methods. They are also in line with several other studies giving interactions between the effects of aging and physical fitness. This study questions the validity of much research on aging, as the data suggest that a more rigorous health screening for biological life events in subjects recruited from the normal, healthy population can reduce performance effects normally ascribed to aging.

Adult↗
PubMed2002

Exercise: a behavioral intervention to enhance brain health and plasticity.

Extensive research on humans suggests that exercise could have benefits for overall health and cognitive function, particularly in later life. Recent studies using animal models have been directed towards understanding the neurobiological bases of these benefits. It is now clear that voluntary exercise can increase levels of brain-derived neurotrophic factor (BDNF) and other growth factors, stimulate neurogenesis, increase resistance to brain insult and improve learning and mental performance. Recently, high-density oligonucleotide microarray analysis has demonstrated that, in addition to increasing levels of BDNF, exercise mobilizes gene expression profiles that would be predicted to benefit brain plasticity processes. Thus, exercise could provide a simple means to maintain brain function and promote brain plasticity.

Acetylcholine↗
PubMed1997

Changes in the ageing brain in health and disease.

The brains of individuals, who are cognitively normal, show age-related changes that include an overall reduction in brain volume and weight, which are associated with gyral atrophy and widening of the sulci of the cerebral cortex, and enlargement of the brain ventricles. These changes are partly the result of nerve cell loss but accurate estimates of neuronal loss are notoriously difficult to make. Microscopically, there are increasing amounts of the age-related pigment, lipofuscin, granulovacuolar degeneration in neurones, Hirano bodies, variable amounts of diffuse deposits of beta-amyloid in the parenchyma, the presence of neurofibrillary tangles mainly confined to the hippocampus and amygdala, and sparse numbers of senile plaques in these brain regions and also in other cortical areas. Of these changes, neurofibrillary tangles and senile plaques are the neuropathological hallmark of Alzheimer's disease in which they are more abundant and widespread. Alzheimer's disease has therefore been regarded as accelerated brain ageing; however, the realization that there is a strong genetic contribution to developing the disease at least implies that it may not be the inevitable, even if frequent, consequence of old age. Understanding the molecular basis of plaque and tangle formation is advancing greatly and is the main focus of research into the cellular and molecular changes observed in the ageing brain.

Alzheimer Disease↗
PubMedDate not supplied

Imaging the neurochemical brain in health and disease.

Neurochemical transmission is a fundamental element of brain organisation that has been relatively unexplored in the living human brain. Continuing advances in radionuclide imaging, particularly positron emission tomography (PET) and single photon emission tomography (SPET), mean that elements of neurochemical transmission can now be directly measured in vivo. With these techniques convincing abnormalities of monoaminergic neurotransmitter systems have been revealed in illnesses such as Parkinson's disease and schizophrenia. Furthermore, mechanisms of drug action and treatment responses can be monitored in vivo. This brief review describes some of our recent attempts to image the neurochemical brain in health and disease at the MRC Cyclotron Unit, Hammersmith Hospital, London.

Adrenergic beta-Antagonists↗
PubMed2026

Loss of ovarian function and estrogen therapy remodel the brain's synaptic and metabolic proteome.

Menopause is linked to cognitive decline and reduced brain metabolism, whereas estrogen (E2) therapy has been shown to mitigate these effects. Understanding the molecular mechanisms by which ovarian hormones and E2 influence neuroprotection is essential for developing strategies to maintain brain health in women. In this study, we examined how the loss of ovarian hormones, with or without E2 treatment, affects the brain proteome and mitochondrial energy production in aged female C57BL/6J mice (36-40 wk). The mice underwent sham or ovariectomy (OVX) surgery and were fed a high-fat diet for 10 wk; 6 wk after surgery, OVX mice received either sesame oil or E2 treatment for 4 wk. Proteomic analysis of brain homogenates revealed 4,992 proteins regulated by E2, with pathway analysis showing increased signaling proteins related to synaptogenesis. OVX reduced proteins involved in synaptic function, branched-chain amino acid and ketone metabolism, the tricarboxylic acid cycle, and oxidative phosphorylation (Complexes I, IV, and V), whereas E2 restored protein expression within these pathways. Despite alterations in OxPhos proteins, basal and state 3 mitochondrial respiration remained unchanged, although notable impairments in Complex IV enzymatic activity were apparent in OVX, which were partially reversed by E2 treatment. Overall, these results indicate that E2 supports brain health by maintaining proteins crucial for synaptic integrity and metabolism, while partially offsetting the functional decline in mitochondrial bioenergetics associated with menopause.NEW & NOTEWORTHY The menopausal transition, marked by declining estrogen levels, alters cognition, neuroplasticity, and brain metabolism. Although hormone therapy benefits cognition, its molecular effects on the brain remain unclear. Using whole-brain proteomics in aged ovariectomized (OVX) mice with or without estrogen treatment, we found that OVX reduced proteins linked to synaptogenesis and mitochondrial metabolism. Estrogen reversed these declines, restoring pathways supporting neuronal signaling and energy balance, identifying estrogen-regulated proteins critical for maintaining brain health during menopause.

Animals↗
PubMedDate not supplied

Cardiovascular diseases, health status, brain imaging findings and neuropsychological functioning in neurologically healthy elderly individuals.

The aim of our study was to evaluate the relationship between health-related factors, brain imaging findings and cognitive functioning. We examined 113 neurologically healthy subjects from 55 to 85 years of age. Health-related variables included a clinical health evaluation, cardiovascular diseases, and other systemic diseases. The presence of white matter changes and cerebral and peripheral atrophy were obtained with magnetic resonance imaging. Neuropsychological tests measuring verbal memory, visual memory, intellectual and language functions, visuoconstructional functions, flexibility, and speed and attention were administered. Results showed that overall health status was not related to cognition. Subjects, who had both arterial hypertension and white matter changes had difficulties in flexibility. Cardiac failure and white matter changes were related to impairment in visuoconstructional functions, flexibility and attention. Significant speed and attention deficits were observed in subjects with cardiac failure and central atrophy. In conclusion, this study verifies the relationship between hypertension, white matter changes and cognitive functions. We found also specific patterns in relation with cardiac failure, brain imaging findings and cognitive functioning, the most vulnerable domains were visuoconstructional functions, flexibility and attention.

Journal Article↗