The pathological basis for the dementia which occurs in 20 to 40% of patients with idiopathic Parkinson's disease (PD) remains uncertain. In the present postmortem study, we compared the prevalence and severity of parenchymal and vascular amyloid-beta (Abeta) deposition in the cerebral cortex in a group of 57 PD brains, including 13 cases with dementia, and in 100 control brains. A higher proportion of PD brains had vascular Abeta deposition, whereas the proportions and severity of parenchymal Abeta were similar in the PD and control groups. There was a poor correlation between Abeta deposition and neurofibrillary tangles which were present in only small numbers in a minority of cases. Cortical Abeta deposition was present in only 6 of the 13 cases with dementia and only 3 fulfilled the Consortium to Establish a Registry for Alzheimer's Disease (CERAD) criteria for definite Alzheimer's disease. The present findings confirm that dementia in PD is only infrequently due to fully established Alzheimer's disease. However, vascular and parenchymal Abeta deposition could still contribute to dementia and cognitive decline when combined with other changes such as alpha-synuclein deposition in the cerebral cortex and cortical Lewy bodies.
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http://dx.doi.org/10.1002/mds.10295 | DOI Listing |
Arq Neuropsiquiatr
January 2025
Second Medical University, School of Clinical Medicine, Weifang Shandong Province, China.
Alzheimer's disease (AD), diabetic cognitive impairment (DCI), and vascular dementia (VD) are considered the most common causes of severe cognitive impairment in clinical practice. Numerous factors can influence their progression, and many studies have recently revealed that metabolic disorders play crucial roles in the progression of cognitive impairment. Mounting evidence indicate that the regulation of lipid metabolism is a major factor in maintaining brain homeostasis.
View Article and Find Full Text PDFAlzheimer's disease (AD) is the most prevalent neurodegenerative dementia, marked by progressive cognitive decline and memory impairment. Despite advances in therapeutic research, single-target-directed treatments often fall short in addressing the complex, multifactorial nature of AD. This arises from various pathological features, including amyloid-β (Aβ) aggregate deposition, metal ion dysregulation, oxidative stress, impaired neurotransmission, neuroinflammation, mitochondrial dysfunction, and neuronal cell death.
View Article and Find Full Text PDFACS Chem Neurosci
January 2025
Department of Health Service, Polyclinic, Sector 6, Jhajjar, Haryana 124103, India.
Alzheimer's disease (AD) impacts millions of elderly adults worldwide causing cognitive decline and severe deterioration of activities of daily life. The popular causal hypotheses for several decades include beta-amyloid (Aβ) deposition and tau hyperphosphorylation. AD research and more than 34% of clinical trials in AD are based on these two hypotheses.
View Article and Find Full Text PDFBiomed Pharmacother
January 2025
Health Sciences Institute of China Medical University, Shenyang 110122, China. Electronic address:
Recently study has found a new form of copper-dependent death called cuproptosis, which differs from apoptosis, ferroptosis, and necrosis. The main process of cuproptosis is copper directly combined with lipid-acetylated proteins in the TCA cycle of mitochondrial response, leading to the aggregation of lipid-acetylated proteins and the loss of Fe-S cluster proteins, resulting in mitochondrial dysfunction, and eventually causing cell death. Previous studies demonstrated that an imbalance in copper homeostasis exacerbates the pathological progression of Alzheimer's disease (AD) through the induction of oxidative stress, inflammatory response, and the accumulation of Aβ deposition and tau protein hyperphosphorylation.
View Article and Find Full Text PDFAlzheimers Dement
January 2025
Center for Geriatric Medicine, Key Laboratory of Alzheimer's Disease of Zhejiang Province, The First Affiliated Hospital and Institute of Aging, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Introduction: Interferon-induced transmembrane protein 3 (IFITM3) modulates γ-secretase in Alzheimer's Disease (AD). Although IFITM3 knockout reduces amyloid β protein (Aβ) production, its cell-specific effect on AD remains unclear.
Methods: Single nucleus RNA sequencing (snRNA-seq) was used to assess IFITM3 expression.
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