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Basic Science and Pathogenesis.
Alzheimers Dement
December 2024
Shanghai Institute of Organic Chemistry, Chinese Academy of Sciences, Shanghai, Shanghai, China.
Background: Pathological tau plays critical roles in many neurodegenerative diseases (NDD), including Alzheimer's disease (AD). However, the mechanisms underlying the initial tau pathogenesis are largely unknown. Extensive tau pathology has been observed in the brains with chronic traumatic encephalopathy (CTE), suggesting repeated traumatic brain injury (rTBI) correlates with tau pathogenesis.
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Alzheimers Dement
December 2024
Department of Bionano Technology, Gachon University, Seongnam, Korea, Republic of (South).
Background: Clusterin, a multifunctional glycoprotein, is implicated in Alzheimer's disease (AD) pathogenesis due to its roles in Aβ aggregation and clearance. Hence, understanding the specific interactions between Clusterin and Aβ would be a crucial for unraveling AD mechanisms and exploring therapeutic avenues. Previous study reported that clusterin bound with Aβ directly.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
University of California San Francisco, San Francisco, CA, USA.
Background: The direct and chaperone-associated interactions of E3 ubiquitin ligase CHIP with tau in Alzheimer's disease and other tauopathies, regulates tau turnover, by directly linking it to ubiquitination and proteasomal degradation, as well as through suppression of tau aggregation. Modulation of these CHIP-driven tau clearance mechanisms can be an effective treatment strategy. Antigen-binding antibody fragments (Fabs) are potent tools that can highly-selectively engage target proteins and act as functional probes or inhibitors.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Tulane University, New Orleans, LA, USA.
Background: It is well established that genetic factors are implicated in the development of Alzheimer's disease (AD), but there is growing interest in how environmental factors like infection contribute to its progression. Recent evidence suggests that greater exposure to infections across the lifespan can potentiate the rate and severity of cognitive decline. In addition to contributing to mechanisms underlying the aggregation of Aβ fragments and phosphorylation of tau proteins, the infectious etiology of dementia may be caused by infectious agents triggering neuroinflammatory pathways and degradation of the blood-brain barrier (BBB).
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
University of Washington, Seattle, WA, USA.
Background: Genetic variation of lysosomal protein, transmembrane protein 106B (TMEM106B) has long been known as a risk factor for a diverse range of neurodegenerative disorders, especially FTLD with progranulin (GRN) haplo-insufficiency, though the mechanisms involved are not yet understood. Recently, through advances in cryo-electron microscopy (cryo-EM), aggregates of the C-Terminal domain of TMEM106B (TMEM CT) were shown to make up previously unidentifiable protein aggregates in the brains of human FTLD, AD, progressive supranuclear palsy (PSP), and dementia with Lewy Bodies (DLB) patients.
Methods: To determine the TMEM CT aggregation propensity and neurodegenerative potential, we generated a new transgenic C.
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