Potential Protective Mechanisms of S-equol, a Metabolite of Soy Isoflavone by the Gut Microbiome, on Cognitive Decline and Dementia DOI Open Access
Akira Sekikawa,

Whitney Wharton,

Brittany Butts

et al.

International Journal of Molecular Sciences, Journal Year: 2022, Volume and Issue: 23(19), P. 11921 - 11921

Published: Oct. 7, 2022

S-equol, a metabolite of soy isoflavone daidzein transformed by the gut microbiome, is most biologically potent among all isoflavones and their metabolites. Soy are phytoestrogens exert actions through estrogen receptor-β. Epidemiological studies in East Asia, where regularly consumed, show that dietary intake inversely associated with cognitive decline dementia; however, randomized controlled trials Western countries did not generally benefit. The discrepant results may be attributed to S-equol production capability; after consuming isoflavones, 40–70% Asians produce whereas 20–30% Westerners do. Recent observational clinical Japan but multiple vascular pathologies, contributing impairment dementia, including arterial stiffness white matter lesion volume. has better permeability blood–brain barrier than although affinity receptor-β similar. also antioxidant known isoflavones. Although available as supplement, no long-term humans have examined effect supplementation on stiffness, cerebrovascular disease, decline, or dementia.

Language: Английский

Alzheimer disease DOI
David S. Knopman, Hélène Amieva, Ronald C. Petersen

et al.

Nature Reviews Disease Primers, Journal Year: 2021, Volume and Issue: 7(1)

Published: May 13, 2021

Language: Английский

Citations

1533
One-Year Trajectory of Cognitive Changes in Older Survivors of COVID-19 in Wuhan, China DOI Open Access

Yu-Hui Liu,

Yang Chen, Qinghua Wang

et al.

JAMA Neurology, Journal Year: 2022, Volume and Issue: 79(5), P. 509 - 509

Published: March 8, 2022

Importance

Determining the long-term impact of COVID-19 on cognition is important to inform immediate steps in research and health policy.

Objective

To investigate 1-year trajectory cognitive changes older survivors.

Design, Setting, Participants

This cohort study recruited 3233 survivors 60 years who were discharged from 3 COVID-19–designated hospitals Wuhan, China, February 10 April 10, 2020. Their uninfected spouses (N = 466) as a control population. Participants with preinfection impairment, concomitant neurological disorder, or family history dementia excluded, well those severe cardiac, hepatic, kidney disease any kind tumor. Follow-up monitoring functioning decline took place at 6 12 months. A total 1438 438 individuals included final follow-up. was categorized nonsevere following American Thoracic Society guidelines.

Main Outcomes Measures

The main outcome change 1 year after patient discharge. Cognitive during first second 6-month follow-up periods assessed using Informant Questionnaire Decline Elderly Telephone Interview Status-40, respectively. Based observed 2 periods, trajectories classified into 4 categories: stable cognition, early-onset decline, late-onset progressive decline. Multinomial conditional logistical regression models used identify factors associated risk

Results

Among 1317 screened, participants treated for (691 male [48.05%] 747 female [51.95%]; median [IQR] age, 69 [66-74] years) (222 [50.68%] 216 [49.32%]; 67 completed 12-month incidence impairment months discharge 12.45%. Individuals cases had lower Status-40 scores than (median [IQR]: severe, 22.50 [16.00-28.00]; nonsevere, 30.00 [26.00-33.00]; control, 31.00 [26.00-33.00]). Severe higher (odds ratio [OR], 4.87; 95% CI, 3.30-7.20), (OR, 7.58; 3.58-16.03), 19.00; 9.14-39.51), while 1.71; 1.30-2.27) when adjusting sex, education level, body mass index, comorbidities.

Conclusions Relevance

In this study, survival an increase longitudinal highlighting importance measures deal challenge.

Language: Английский

Citations

192
Vascular Cognitive Impairment (VCI) DOI Creative Commons
Tatjana Rundek, Magdalena I. Tolea, Taylor Ariko

et al.

Neurotherapeutics, Journal Year: 2021, Volume and Issue: 19(1), P. 68 - 88

Published: Dec. 22, 2021

Vascular cognitive impairment (VCI) is predominately caused by vascular risk factors and cerebrovascular disease. VCI includes a broad spectrum of disorders, from mild to dementia ischemic or hemorrhagic stroke, alone in combination with neurodegeneration including Alzheimer's disease (AD) AD-related dementia. accounts for at least 20-40% all diagnosis. Growing evidence indicates that pathology the most important contributor dementia, additive synergistic interactions neurodegenerative pathology. The common underlying mechanism chronic age-related dysregulation CBF, although other such as inflammation cardiovascular dysfunction play role. are prevalent if measured midlife they predict later life. Particularly, hypertension, high cholesterol, diabetes, smoking each associated 20 40% increased Control these multimodality strategies an inclusion lifestyle modification promising strategy treatment prevention VCI. In this review, we present recent developments VCI, its mechanisms, diagnostic criteria, neuroimaging correlates, determinants, current intervention We have also summarized relevant literature field

Language: Английский

Citations

176
Astrocyte Activation in Neurovascular Damage and Repair Following Ischaemic Stroke DOI Open Access
Adjanie Patabendige, Ayesha Singh, Stuart I. Jenkins

et al.

International Journal of Molecular Sciences, Journal Year: 2021, Volume and Issue: 22(8), P. 4280 - 4280

Published: April 20, 2021

Transient or permanent loss of tissue perfusion due to ischaemic stroke can lead damage the neurovasculature, and disrupt brain homeostasis, causing long-term motor cognitive deficits. Despite promising pre-clinical studies, clinically approved neuroprotective therapies are lacking. Most studies have focused on neurons while ignoring important roles other cells neurovascular unit, such as astrocytes pericytes. Astrocytes for development maintenance blood–brain barrier, structural support, control cerebral blood flow secretion factors. Emerging data suggest that astrocyte activation exerts both beneficial detrimental effects following stroke. Activated provide neuroprotection contribute neurorestoration, but also secrete inflammatory modulators, leading aggravation lesion. more resistant than cell types pathology, exert a regulative effect in response ischaemia. These remain incompletely understood, though they represent an appealing target protection In this review, we summarise astrocytic contributions repair stroke, explore mechanisms promote revascularisation which may be targeted developing novel

Language: Английский

Citations

145
Vascular contributions to Alzheimer's disease DOI Creative Commons
Laura Eisenmenger,

Anthony Peret,

Bolanle M. Famakin

et al.

Translational research, Journal Year: 2022, Volume and Issue: 254, P. 41 - 53

Published: Dec. 15, 2022

Language: Английский

Citations

79
Forecasting the Burden of Cardiovascular Disease and Stroke in the United States Through 2050—Prevalence of Risk Factors and Disease: A Presidential Advisory From the American Heart Association DOI
Karen E. Joynt Maddox, Mitchell S.V. Elkind, Hugo J. Aparicio

et al.

Circulation, Journal Year: 2024, Volume and Issue: 150(4)

Published: June 4, 2024

BACKGROUND: Cardiovascular disease and stroke are common costly, their prevalence is rising. Forecasts on the of risk factors clinical events crucial. METHODS: Using 2015 to March 2020 National Health Nutrition Examination Survey 2019 Medical Expenditure Panel Survey, we estimated trends in for cardiovascular based adverse levels Life’s Essential 8 stroke. We projected through 2050, overall by age race ethnicity, accounting changes demographics. RESULTS: estimate that among adults, hypertension will increase from 51.2% 61.0% 2050. Diabetes (16.3% 26.8%) obesity (43.1% 60.6%) increase, whereas hypercholesterolemia decline (45.8% 24.0%). The prevalences poor diet, inadequate physical activity, smoking improve over time, sleep worsen. Prevalences coronary (7.8% 9.2%), heart failure (2.7% 3.8%), (3.9% 6.4%), atrial fibrillation (1.7% 2.4%), total (11.3% 15.0%) rise. Clinical CVD affect 45 million including more than 184 adults 2050 (>61%). Similar children. Most be worse people identifying as American Indian/Alaska Native or multiracial, Black, Hispanic. CONCLUSIONS: many most established diseases next 30 years. public health interventions needed effectively manage, stem, even reverse these trends.

Language: Английский

Citations

65
Hippocampal Vascular Supply and Its Role in Vascular Cognitive Impairment DOI Open Access

Abbie C. Johnson

Stroke, Journal Year: 2023, Volume and Issue: 54(3), P. 673 - 685

Published: Feb. 27, 2023

The incidence of age-related dementia is increasing as the world population ages and due to lack effective treatments for dementia. Vascular contributions cognitive impairment are prevalence pathologies associated with cerebrovascular disease rise, including chronic hypertension, diabetes, ischemic stroke. hippocampus a bilateral deep brain structure that central learning, memory, function highly susceptible hypoxic/ischemic injury. Compared cortical regions such somatosensory cortex, less known about hippocampal vasculature critical in maintaining neurocognitive health. This review focuses on vascular supply, presenting what hemodynamics blood-brain barrier during health disease, discusses evidence supports its contribution Understanding vascular-mediated injury contributes memory dysfunction healthy aging essential develop slow decline. may represent one therapeutic target mitigate epidemic.

Language: Английский

Citations

61
Exposome and unhealthy aging: environmental drivers from air pollution to occupational exposures DOI Creative Commons

Tamás Pándics,

Dávid Major, Vince Fazekas‐Pongor

et al.

GeroScience, Journal Year: 2023, Volume and Issue: 45(6), P. 3381 - 3408

Published: Sept. 9, 2023

The aging population worldwide is facing a significant increase in age-related non-communicable diseases, including cardiovascular and brain pathologies. This comprehensive review paper delves into the impact of exposome, which encompasses totality environmental exposures, on unhealthy aging. It explores how factors contribute to acceleration processes, biological age, facilitate development progression wide range age-associated diseases. cognitive health chronic diseases affecting system central nervous discussed, with specific focus Alzheimer's disease, Parkinson's stroke, small vessel vascular impairment (VCI). Aging major risk factor for these Their pathogenesis involves cellular molecular mechanisms such as increased oxidative stress, impaired mitochondrial function, DNA damage, inflammation influenced by factors. Environmental toxicants, ambient particulate matter, pesticides, heavy metals, organic solvents, have been identified contributors disorders. These toxicants can inflict both macro- microvascular damage many them also cross blood-brain barrier, inducing neurotoxic effects, neuroinflammation, neuronal dysfunction. In conclusion, play critical role modulating A deeper understanding exacerbate processes neurodegenerative VCI, dementia crucial preventive strategies interventions promote cardiovascular, cerebrovascular, health. By mitigating exposure harmful promoting healthy aging, we strive reduce burden pathologies population.

Language: Английский

Citations

46
Sex-specific mechanisms in vascular aging: exploring cellular and molecular pathways in the pathogenesis of age-related cardiovascular and cerebrovascular diseases DOI Creative Commons
Anna Ungvari, Rafał Gulej, Roland Patai

et al.

GeroScience, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 3, 2025

Language: Английский

Citations

3
Dysregulation of Systemic Immunity in Aging and Dementia DOI Creative Commons

Jenny Lutshumba,

Barbara S. Nikolajczyk, Adam D. Bachstetter

et al.

Frontiers in Cellular Neuroscience, Journal Year: 2021, Volume and Issue: 15

Published: June 22, 2021

Neuroinflammation and the tissue-resident innate immune cells, microglia, respond contribute to neurodegenerative pathology. Although microglia have been focus of work linking neuroinflammation associated dementias like Alzheimer’s Disease, inflammatory milieu brain is a conglomerate cross-talk amongst systemic cells soluble mediators cytokines. Age-related changes in profile at levels both periphery are largely orchestrated by system cells. Strong evidence indicates that adaptive latter including T B chronic thus dementia. Neurodegenerative hallmarks coupled with more traditional stimuli infection or injury likely combine trigger maintain persistent microglial inflammation. This review summarizes age-related cell function, special emphasis on lymphocytes as source inflammation, discusses how such may potentiate central nervous inflammation culminate We recap understudied area AD-associated greater detail provide unifying perspective inflammation-fueled dementia, an eye toward two-way communication between parenchyma blood focused our human subjects studies, adding key data from animal models relevant.

Language: Английский

Citations

81