Utility of combined plasma amyloid beta 40, amyloid beta 42, total tau, and NfL along with a measure of cognitive functioning in detecting cognitive impairment among Hispanic, Mexican Americans compared to non‐Hispanic whites

Physical activity has an unquestionable impact on broadly understood human health. One interesting issue related to this is the importance of movement on mental health and cognitive functioning. Research shows that regular physical activity improves the cognitive functioning of adults and people with mental disorders. Regular physical activity can be an important and powerful protective factor in cognitive impairment and dementia in the elderly, and exercise is an important non-pharmacological treatment for mild cognitive impairment or neurodegenerative diseases. This study aims to present the impact of physical activity on selected cognitive functions in physically active women over 60 years of age. The research was carried out in a group of 110 generally healthy women from the area of western Poland over 60 years of age, who were divided into four groups based on the intensity of their physical activity. A pedometer (sport watch) and a physical activity diary were used to measure physical activity. Body Mass Index was assessed. Selected cognitive functions were assessed using the MMSE test, motor and psychomotor skills were measured, and Luria’s auditory memory test and recall test, a clock drawing test, and a GDS test were performed. There were statistically significant relationships between the level of physical activity and the effectiveness of cognitive processes. These results show that about 5000 steps a day is enough to see a positive effect on the mental health and cognitive functioning of this group of the elderly population. The women had an average BMI of 28.1 ± 4.7. BMI, indicating an overweight condition (over 30 kg/m2), was observed in 31% of women. The results of this study lead the authors to conclude that physical activity positively influences cognitive function and can be recommended for all seniors who do not have other serious comorbidities that would prevent them from playing sports.

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Functional genomic analyses uncover APOE-mediated regulation of brain and cerebrospinal fluid beta-amyloid levels in Parkinson disease

Acta Neuropathologica Communications ◽

10.1186/s40478-020-01072-8 ◽

2020 ◽

Vol 8 (1) ◽

Author(s):

Laura Ibanez ◽

Jorge A. Bahena ◽

Chengran Yang ◽

Umber Dube ◽

Fabiana H. G. Farias ◽

...

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Amyloid Beta ◽

Alpha Synuclein ◽

Phosphorylated Tau ◽

Polygenic Risk ◽

Total Tau ◽

Genomic Architecture ◽

Genome Wide ◽

Csf Biomarker

AbstractAlpha-synuclein is the main protein component of Lewy bodies, the pathological hallmark of Parkinson’s disease. However, genetic modifiers of cerebrospinal fluid (CSF) alpha-synuclein levels remain unknown. The use of CSF levels of amyloid beta1–42, total tau, and phosphorylated tau181 as quantitative traits in genetic studies have provided novel insights into Alzheimer’s disease pathophysiology. A systematic study of the genomic architecture of CSF biomarkers in Parkinson’s disease has not yet been conducted. Here, genome-wide association studies of CSF biomarker levels in a cohort of individuals with Parkinson’s disease and controls (N = 1960) were performed. PD cases exhibited significantly lower CSF biomarker levels compared to controls. A SNP, proxy for APOE ε4, was associated with CSF amyloid beta1–42 levels (effect = − 0.5, p = 9.2 × 10−19). No genome-wide loci associated with CSF alpha-synuclein, total tau, or phosphorylated tau181 levels were identified in PD cohorts. Polygenic risk score constructed using the latest Parkinson’s disease risk meta-analysis were associated with Parkinson’s disease status (p = 0.035) and the genomic architecture of CSF amyloid beta1–42 (R2 = 2.29%; p = 2.5 × 10−11). Individuals with higher polygenic risk scores for PD risk presented with lower CSF amyloid beta1–42 levels (p = 7.3 × 10−04). Two-sample Mendelian Randomization revealed that CSF amyloid beta1–42 plays a role in Parkinson’s disease (p = 1.4 × 10−05) and age at onset (p = 7.6 × 10−06), an effect mainly mediated by variants in the APOE locus. In a subset of PD samples, the APOE ε4 allele was associated with significantly lower levels of CSF amyloid beta1–42 (p = 3.8 × 10−06), higher mean cortical binding potentials (p = 5.8 × 10−08), and higher Braak amyloid beta score (p = 4.4 × 10−04). Together these results from high-throughput and hypothesis-free approaches converge on a genetic link between Parkinson’s disease, CSF amyloid beta1–42, and APOE.

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