Background: Alzheimer's disease is a neurodegenerative brain disease resulting from the deterioration of neuronal cells and vascular dementia, the latter of which results from cerebrovascular disorders. Exercise is effective in preventing and treating degenerative brain diseases as it activates blood flow to the brain, increases nerve production in the hippocampus, and promotes the expression of synaptic plasticity-related proteins. Therefore, this study investigated the effects of 16-week aquatic and land-based exercise programs on amyloid beta (Aβ), heat shock protein (HSP) 27 levels, and pulse wave velocity (PWV).
Materials And Methods: Forty elderly women, aged 60-70 years, voluntarily participated in the study. They were divided into control (n = 12), aquatic exercise (n = 14), and land-based exercise groups (n = 14). The variables of amyloid beta, heat shock protein 27, and pulse wave velocity were measured in all the participants before and after the 16-week study.
Results: Significantly higher levels of serum HSP27 (p < 0.05) and significantly lower levels of vascular elasticity (p < 0.05) were found in the aquatic exercise group after 16 weeks of exercise compared with the control group. Aβ did not significantly differ between groups. Thirty minutes after the first exercise, Aβ in the aquatic exercise group (p < 0.01) and HSP27 in the land-based exercise group (p < 0.05) were significantly higher than the corresponding levels in the resting condition before exercise. 30 min after the last exercise, Aβ (p < 0.01) and HSP27 (p < 0.05) were significantly higher.
Conclusions: Aquatic and land-based exercises increased serum Aβ and HSP27 and decreased pulse wave velocity. Thus, they may play a positive role in the prevention of degenerative brain diseases and improvement of brain function in elderly people.
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http://dx.doi.org/10.1016/j.exger.2018.03.024 | DOI Listing |
Geroscience
January 2025
Psychology, School of Social Sciences, Nanyang Technological University, 48 Nanyang Avenue S639818, Singapore, Singapore.
In Alzheimer's disease (AD), the accumulation of neuropathological markers such as amyloid-β plaques, neurofibrillary tangles, and cortical neurodegeneration occurs over many years before overt manifestation of cognitive impairment. There is thus a need for neuropsychological markers that are indicative of pathological changes in the early stages of the disease. Intra-individual cognitive variability (IICV), defined as the variation of an individual's performance across cognitive domains, is a promising neuropsychological marker measuring heterogeneous changes in cognition that may reflect these early pathological changes.
View Article and Find Full Text PDFMol Divers
January 2025
Department of Biophysics, Panjab University, Chandigarh, 160014, India.
Alzheimer's disease (AD) is a degenerative neurological disorder defined by the formation of β-amyloid (Aβ) plaques and neurofibrillary tangles within the brain. Current pharmacological treatments for AD only provide symptomatic relief, and there is a lack of definitive disease-modifying therapies. Chemical chaperones, such as 4-Phenylbutyric acid (4PBA) and Tauroursodeoxycholic acid, have shown neuroprotective effects in animal and cell culture models.
View Article and Find Full Text PDFJ Alzheimers Dis
January 2025
Department of General Internal Medicine, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Background: Alzheimer's disease (AD) is an irreversible age-related neurodegenerative condition characterized by the deposition of amyloid-β (Aβ) peptides and neurofibrillary tangles. Di Huang Yi Zhi (DHYZ) formula, a traditional Chinese herbal compound comprising several prescriptions, demonstrates properties that improve cognitive abilities in clinical. Nonetheless, its molecular mechanisms on treating AD through improving neuron cells mitochondria function have not been deeply investigated.
View Article and Find Full Text PDFAnal Chem
January 2025
State Key Laboratory of Chemical Resource Engineering, College of Chemistry, Beijing University of Chemical Technology, Beijing 100029, China.
The spontaneous aggregation of amyloid-β (Aβ) leads to neuronal cell death in the brain and causes the development of Alzheimer's disease (AD). The efficient detection of the aggregation state of Aβ holds significant promise for the early diagnosis and subsequent treatment of this neurodegenerative disorder. Currently, most of the fluorescent probes used for the detection of Aβ fibrils share similar recognition moieties, such as the ,-dimethylamino group, ,-diethylamino group, and piperidyl group.
View Article and Find Full Text PDFCurr Top Med Chem
January 2025
Department of Histology and Embryology, School of Basic Medicine, Hengyang Medical School, University of South China, Hengyang, 421001, China.
In recent years, an increasing number of studies have shown that increased activation of aspartic endopeptidases (AEPs) is a common symptom in neurodegenerative diseases (NDDs). AEP cleaves amyloid precursor protein (APP), tau (microtubule-associated protein tau), α- synuclein (α-syn), SET (a 39-KDa phosphoprotein widely expressed in various tissues and localizes predominantly in the nucleus), and TAR DNA-binding protein 43 (TDP-43), and promotes their aggregation, contributing to Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease, multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS), and frontotemporal dementia (FTD) pathogenesis. Abundant evidence supports the notion that CCAAT/enhancer-binding protein β (C/EBPβ)/AEP may play an important role in NDDs.
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