Brain atrophy occurs in aging even in the absence of dementia, but it is unclear to what extent this is due to undetected preclinical Alzheimer disease. Here we examine a cross-sectional cohort (ages 18-88) free from confounding influence of preclinical Alzheimer disease, as determined by amyloid PET scans and three years of clinical evaluation post-imaging. We determine the regional strength of age-related atrophy using linear modeling of brain volumes and cortical thicknesses with age. Age-related atrophy was seen in nearly all regions, with greatest effects in the temporal lobe and subcortical regions. When modeling age with the estimated derivative of smoothed aging curves, we found that the temporal lobe declined linearly with age, subcortical regions declined faster at later ages, and frontal regions declined slower at later ages than during midlife. This age-derivative pattern was distinct from the linear measure of age-related atrophy and significantly associated with a measure of myelin. Atrophy did not detectably differ from a preclinical Alzheimer disease cohort when age ranges were matched.
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http://dx.doi.org/10.1016/j.neurobiolaging.2021.09.010 | DOI Listing |
Cureus
December 2024
Research Team for Human Care, Tokyo Metropolitan Institute for Geriatrics and Gerontology, Tokyo, JPN.
Purpose Muscle atrophy progresses with age. The motor function may be estimated by measuring the muscle mass; however, if muscle quality deteriorates due to an increase in connective tissue within the muscle, a decline in motor function may be missed by measuring muscle mass alone. Therefore, it is important to understand the relationship between muscle mass, muscle quality, and motor function.
View Article and Find Full Text PDFExp Gerontol
January 2025
School of Food and Bioengineering, Xihua University, Chengdu 610039, China.
Purpose: The study aims to investigate the therapeutic effects of the aqueous extract of Atractylodes macrocephala Koidz. (AEA) on dexamethasone (Dex) -induced sarcopenia in mice and to explore its possible mechanisms of action.
Methods: This study utilized bioinformatics analysis to explore the primary pathogenic mechanisms of age-related sarcopenia and Dex-induced muscle atrophy.
Front Cell Dev Biol
January 2025
Department of Health Promotion Sciences, Graduated School of Human Health Sciences, Tokyo Metropolitan University, Hachioji, Japan.
Cell therapy of skeletal muscles is a promising approach for the prevention of muscular diseases and age-related muscle atrophy. However, cell transplantation to treat muscle atrophy that does not involve disease, such as sarcopenia, is considered impossible because externally injected cells rarely engraft into non-injured muscle tissue. Additionally, skeletal muscle-specific somatic stem cells, called satellite cells, lose their ability to adhere to tissue after being cultured and transforming into myoblasts.
View Article and Find Full Text PDFJ Physiol
January 2025
Department of Physiology & Biomedical Engineering, Mayo Clinic, Rochester, MN, USA.
Motor neurons (MNs) within the nucleus ambiguus innervate the skeletal muscles of the larynx, pharynx and oesophagus, which are essential for swallow. Disordered swallow (dysphagia) is a serious problem in elderly humans, increasing the risk of aspiration, a key contributor to mortality. Despite this importance, very little is known about the pathophysiology of ageing dysphagia and the relative importance of frank muscle weakness compared to timing/activation abnormalities.
View Article and Find Full Text PDFJ Neuropathol Exp Neurol
January 2025
Department of Biological Sciences, Delaware State University, Dover, DE, United States.
Trans-active response DNA-binding protein-43 (TDP-43) is the major pathological protein in motor neuron disease and TDP-43 pathology has been described in the brains of up to 50% of patients with Alzheimer disease (AD). Hippocampal sclerosis of aging (HS-A), an age-related neuropathology characterized by severe neuronal loss and gliosis in CA1 and/or subiculum, is found in ∼80% of cases that are positive for phosphorylated TDP-43. HS-A is seen as a co-pathology in cases with AD, limbic-predominant age-related TDP-43 encephalopathy neuropathologic changes (LATE-NC), and frontotemporal degeneration.
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