Ankerborg6589
orks and the role higher-level cognitive processes and spatial perception/processing play in postural control.
Transmissible spongiform encephalopathies (TSEs) are rare neurodegenerative disorders that affect animals and humans. Bovine spongiform encephalopathy (BSE) in cattle, and Creutzfeld-Jakob Disease (CJD) in humans belong to this group. The causative agent of TSEs is called "prion", which corresponds to a pathological form (PrPSc) of a normal cellular protein (PrPC) expressed in nerve cells. PrPSc is resistant to degradation and can induce abnormal folding of PrPC, and TSEs are characterized by extensive spongiosis and gliosis and the presence of PrPSc amyloid plaques. CJD presents initially with clinical symptoms similar to Alzheimer's disease (AD). In AD, tau aggregates and amyloid-β protein plaques are associated with memory loss and cognitive impairment in patients.
In this work, we study the role of tau and its relationship with PrPSc plaques in CJD.
Multiple immunostainings with specific antibodies were carried out and analyzed by confocal microscopy.
We found increased expression of the glial fibrillary acidic protein (GFAP) and matrix metalloproteinase (MMP-9), and an exacerbated apoptosis in the granular layer in cases with prion disease. In these cases, tau protein phosphorylated at Thr-231 was overexpressed in the axons and dendrites of Purkinje cells and the extensions of parallel fibers in the cerebellum.
We conclude that phosphorylation of tau may be a response to a toxic and inflammatory environment generated by the pathological form of prion.
We conclude that phosphorylation of tau may be a response to a toxic and inflammatory environment generated by the pathological form of prion.
Heart failure has been considered as a potential modifiable risk factor for cognitive impairment and dementia. Left ventricular ejection fraction (LVEF), an indicator of cardiac dysfunction, has also been associated with cognitive aging. However, the effect of LVEF on Alzheimer's disease (AD) pathology is still less known.
We aimed to investigate the associations of LVEF with cerebrospinal fluid (CSF) biomarkers for AD in cognitively normal elders.
A total of 423 cognitively normal individuals without heart failure were included from the Chinese Alzheimer's Biomarker and LifestylE (CABLE) study. Participants were divided into low LVEF group (50%≤LVEF < 60%) and high LVEF group (LVEF≥60%). The associations of LVEF with CSF AD biomarkers including CSF amyloid-β 42 (Aβ42), total-tau (t-tau), and phosphorylated tau (p-tau) were analyzed using multivariate linear regression models.
Participants with low LVEF had higher levels of CSF t-tau (β= -0.009, p = 0.006) and t-tau/Aβ42 ratios (β= -0.108, p = 0.026). Subgroup analyses showed that the associations only existed in female and middle-aged groups (< 65 years old). Besides, participants with low LVEF had higher levels of CSF p-tau (β= -0.002, p = 0.043) in middle-aged group.
In conclusion, our findings revealed the associations between LVEF and AD pathology, which may provide new insights into AD prevention through maintaining cardiac function.
In conclusion, our findings revealed the associations between LVEF and AD pathology, which may provide new insights into AD prevention through maintaining cardiac function.
Cerebral microbleed (CMB) is an increasingly important risk factor for cognitive impairment due to population aging. Controversies, however, remain regarding the exact association between CMB and cognitive dysfunction.
We aimed to determine the relationship between CMB burden and cognitive impairment, and also explore the characteristics of cognitive decline in CMB patients for middle-aged and elderly people.
The present cross-sectional study included 174 participants (87 CMB patients and 87 controls) who underwent brain magnetic resonance imaging and a battery of neuropsychological test. Global cognitive function was measured using Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment (MoCA). Compound z-scores were calculated for three cognitive subdomains memory, executive function and processing speed.
CMB patients had lower scores of MMSE (p < 0.001) and MoCA (p < 0.001). Patients at each category of CMB count had worse performance in global cognitive function and all three ive dysfunction is causal.
Larger, more active social networks are estimated to be associated with lower risks of cognitive decline. see more However, roles of various social relationships in a broad social network in protecting against cognitive decline remain to be elucidated.
We aimed to investigate how social roles within a social network and number of social network members are associated with cognitive decline.
Six waves of National Health and Aging Trends Study (2011-2016, NHATS) were utilized to examine the development of mild cognitive impairment (MCI) and probable dementia determined using validated criteria. link2 Multivariable-adjusted multi-state survival models were used to model incidences and transitions, jointly with misclassification errors.
A total of 6,078 eligible NHATS participants were included (average age 77.49±7.79 years; female 58.42%; non-Hispanic white 68.99%). Multivariable-adjusted analyses revealed that having more social network members was associated with lower hazards of conversion from MCI to probable dementia (adjusted Hazard Ratio; aHR = 0.82; 95%confidence intervals; 95%CI = [0.67-0.99]), meanwhile having at least one college-educated family member within a social network was associated with lower incidence of probable dementia (aHR = 0.37 [0.26-0.51]). Having at least one friend within a social network was associated with a lower hazard of incidence of probable dementia (aHR = 0.48 [0.33-0.71]), but a higher risk of mortality in the MCI group (aHR = 2.58 [1.47-4.51]).
Having more social network members, having at least one friend, and having at least one college-educated family member within a social network, were associated with lower risks of incidence of dementia or conversion from MCI to dementia.
Having more social network members, having at least one friend, and having at least one college-educated family member within a social network, were associated with lower risks of incidence of dementia or conversion from MCI to dementia.
Serum uric acid (SUA) affects the reaction of oxidative stress and free radicals in the neurodegenerative processes. However, whether SUA impacts Alzheimer's disease (AD) pathology remains unclear.
We aimed to explore whether high SUA levels can aggravate the neurobiological changes of AD in preclinical AD.
We analyzed cognitively intact participants (n = 839, age 62.16 years) who received SUA and cerebrospinal fluid (CSF) biomarkers (amyloid-β [Aβ], total tau [t-Tau], and phosphorylated tau [p-Tau]) measurements from the Chinese Alzheimer's Biomarker and LifestylE (CABLE) database using multivariable-adjusted linear models.
Levels of SUA in the preclinical AD elevated compared with the healthy controls (p = 0.007) and subjects with amyloid pathology had higher concentration of SUA than controls (p = 0.017). Roughly, equivalent levels of SUA displayed among cognitively intact individuals with or without tau pathology and neurodegeneration. CSF Aβ1-42 (p = 0.019) and Aβ1-42/Aβ1-40 (p = 0.027) were decreased and CSF p-Tau/Aβ1-42 (p = 0.009) and t-Tau/Aβ1-42 (p = 0.043) were increased with the highest (> 75th percentile) SUA when compared to lowest SUA, implying a high burden of cerebral amyloidosis in individuals with high SUA. Sensitivity analyses using the usual threshold to define hyperuricemia and precluding drug effects yielded robust associations. Nevertheless, the quadratic model did not show any U-shaped relationships between them.
SUA may aggravate brain amyloid deposition in preclinical AD, which corroborated the detrimental role of SUA.
SUA may aggravate brain amyloid deposition in preclinical AD, which corroborated the detrimental role of SUA.
Neighborhood greenness (vegetative presence) has been linked to multiple health outcomes, but its relationship to Alzheimer's disease (AD) and non-Alzheimer's (non-AD) dementia has been less studied.
This study examines the relationship of greenness to both AD and non-AD dementia in a population-based sample of Medicare beneficiaries.
Participants were 249,405 US Medicare beneficiaries aged > 65 years living in Miami-Dade County, FL, from 2010 to 2011. Multi-level analyses examined the relationship of greenness, assessed by mean Census block level Normalized Difference Vegetation Index (NDVI), to odds of each of AD, Alzheimer's disease and related dementias (ADRD), and non-AD dementia, respectively. Covariates included age, gender, race/ethnicity, number of comorbid health conditions, and neighborhood income.
Higher greenness was associated with reduced risk of AD, ADRD, and non-AD dementia, respectively, adjusting for individual and neighborhood sociodemographics. Compared to the lowest greenness tertile, the highest greenness tertile was associated with reduced odds of AD by 20%(odds ratio, 0.80; 95%CI, 0.75-0.85), ADRD by 18%(odds ratio, 0.82; 95%CI, 0.77-0.86), and non-AD dementia by 11%(odds ratio, 0.89; 95%CI, 0.82-0.96). After further adjusting for number of comorbidities, compared to the lowest greenness tertile, the highest greenness tertile was associated with reduced odds of AD (OR, 0.94; 95%CI, 0.88-1.00) and ADRD (OR, 0.93; 95%CI, 0.88-0.99), but not non-AD dementia (OR, 1.01; 95%CI, 0.93-1.08).
High neighborhood greenness may be associated with lower odds of AD and ADRD. Environmental improvements, such as increasing neighborhood vegetation, may be a strategy to reduce risk for AD and possibly other dementias.
High neighborhood greenness may be associated with lower odds of AD and ADRD. Environmental improvements, such as increasing neighborhood vegetation, may be a strategy to reduce risk for AD and possibly other dementias.
Few studies have compared factors related to cognitive function among people with similar genetic backgrounds but different lifestyles.
We aimed to identify factors related to lower cognitive scores among older Japanese men in two genetically similar cohorts exposed to different lifestyle factors.
This cross-sectional study of community-dwelling Japanese men aged 71-81 years included 2,628 men enrolled in the Kuakini Honolulu-Asia Aging Study based in Hawaii and 349 men in the Shiga Epidemiological Study of Subclinical Atherosclerosis based in Japan. We compared participant performance through Cognitive Abilities Screening Instrument (CASI) assessment in Hawaii (1991-1993) and Japan (2009-2014). Factors related to low cognitive scores (history of cardiovascular disease, cardiometabolic factors, and lifestyle factors) were identified with questionnaires and measurements. Multivariable logistic regression analysis was used to calculate the adjusted odds ratios (ORs) of a low (< 82) CASI score based on among genetically similar older men exposed to different lifestyle factors.
Social apathy, a reduction in initiative in proposing or engaging in social activities or interactions, is common in mild neurocognitive disorders (MND). link3 Current apathy assessment relies on self-reports or clinical scales, but growing attention is devoted to defining more objective, measurable and non-invasive apathy proxies.
In the present study we investigated the interest of recording action kinematics in a social reach-to-grasp task for the assessment of social apathy.
Thirty participants took part in the study 11 healthy controls (HC; 6 females, mean age = 68.3±10.5 years) and 19 subjects with MND (13 females, mean age = 75.7±6.3 years). Based on the Diagnostic Criteria for Apathy, MND subjects were classified as socially apathetic (A-MND, N = 9) versus non-apathetic (NA-MND, N = 10). SensRing, a ring-shaped wearable sensor, was placed on their index finger, and subjects were asked to reach and grasp a can to place it into a cup (individual condition) and pass it to a partner (social condition).
In the reach-to-grasp phase of the action, HC and NA-MND showed different acceleration and velocity profiles in the social versus individual condition.
