Previous studies showed that functional connectivity (FC) within resting state (RS) networks is modulated by previous experience. In this study the effects of sustained cognitive performance on subsequent RS FC were investigated in healthy young (25-30 years; n=15) and middle-aged (50-60 years; n=14) male schoolteachers. Participants were scanned (functional magnetic resonance imaging [MRI]) after a cognitively demanding and a control intervention (randomized tester-blind within-subject design). Independent component analysis (ICA) was used to decompose the data into spatially independent networks. This study focused on the executive control (ExN), the left and right frontoparietal (FPN), and the default mode network (DMN). The effects of cognitive performance and age were calculated with a full-factorial analysis of variance (ANOVA). A main effect of age was found in the left inferior frontal gyrus for the ExN and in the middle frontal gyrus for the DMN with middle-aged teachers having reduced RS FC. Sustained cognitive performance increased subsequent RS FC between the ExN and a lingual/parahippocampal cluster, and between the left FPN and a right calcarine/precuneus cluster. In these clusters, FC strength correlated positively with the perceived amount of effort during the intervention. Further, sustained cognitive performance affected subsequent RS FC between the ExN and the right temporal superior gyrus differently in young and middle-aged men. The results suggest that effects of age on RS FC are already present at middle age. Sustained cognitive performance increased RS FC between task-positive networks and other brain regions, although a change in RS FC within the networks was not found.
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http://dx.doi.org/10.1089/brain.2011.0060 | DOI Listing |
PLoS One
January 2025
Department of Sport Studies, Faculty of Education Studies, Universiti Putra Malaysia, Selangor, Malaysia.
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December 2024
USC School of Pharmacy, Los Angeles, CA, USA.
Background: Cellular senescence is a hallmark of aging and has been implicated in several neurodegenerative diseases including Alzheimer's disease (AD). Senescence cells undergo changes in gene expression and metabolism and can exhibit a so-called "senescence-associated secretory phenotype" (SASP) characterized by increased secretion of pro-inflammatory molecules and factors which can damage nearby cells, contributing to AD pathology progression.
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Alzheimers Dement
December 2024
University of Pittsburgh, Pittsburgh, PA, USA.
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View Article and Find Full Text PDFAlzheimers Dement
December 2024
Department of Pediatrics, Division of Infectious Diseases and Immunology, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Background: Alzheimer's disease (AD) is a progressive irreversible dementia characterized by beta-amyloid protein plaque deposition and hyperphosphorylation of tau forming neurofibrillary tangles, and neurodegeneration. An emerging theory posits that infections could be one of the triggering factors in AD development and progression. Multiple lines of evidence have linked Chlamydia pneumoniae (Cp), a gram-negative obligate intracellular bacterium with AD.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Carnegie Mellon University, Pittsburgh, PA, USA.
Background: The failure of amyloid plaque-reducing drugs to reverse cognitive decline in Alzheimer's disease (AD) has suggested that treatments might be more effective in early or prodromal stages of the disease. However, the progression of synaptic and circuit changes associated with Aβ overexpression, particularly at very early ages, have not been well-characterized. Indeed, evidence from both human and animal studies indicates that brain structure and function might be altered months to years before plaques can be detected.
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