Co-Aggregation of TDP-43 with Other Pathogenic Proteins and Their Co-Pathologies in Neurodegenerative Diseases DOI Open Access
Lei‐Lei Jiang,

Xiangle Zhang,

Hongyu Hu

et al.

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(22), P. 12380 - 12380

Published: Nov. 18, 2024

Pathological aggregation of a specific protein into insoluble aggregates is common hallmark various neurodegenerative diseases (NDDs). In the earlier literature, each NDD characterized by one or two pathogenic proteins, which can serve as disease-specific biomarkers. The these proteins thought to be major cause deleterious result in most NDDs. However, accumulating evidence shows that interact and co-aggregate with other different NDDs, thereby contributing disease onset progression synergistically. During past years, more than type has been found co-exist some individuals, may increase complexity pathogenicity diseases. This article reviews discusses biochemical characteristics molecular mechanisms underlying co-aggregation co-pathologies associated TDP-43 pathology. aggregates, amyotrophic lateral sclerosis (ALS) frontotemporal lobar degeneration (FTLD), often detected such Alzheimer's (AD), Parkinson's (PD), Huntington's (HD) spinocerebellar ataxia 2 (SCA2). many cases, shown multiple vitro vivo. Furthermore, co-occurrence have important consequences aggravate Thus, current viewpoint NDDs their relevance gain insights patho-mechanisms therapeutic potential

Language: Английский

Hippocampal neuronal loss and cognitive decline in LATE‐NC and ADNC among community‐dwelling older persons DOI Creative Commons
Sonal Agrawal, Lei Yu, Sue E. Leurgans

et al.

Alzheimer s & Dementia, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 30, 2025

Abstract INTRODUCTION This study investigates the inter‐related roles of hippocampal neuronal loss (HNL), limbic‐predominant age‐related TAR‐DNA binding protein 43 kDa (TDP‐43) encephalopathy neuropathologic changes (LATE‐NC), and Alzheimer's disease (ADNC) on cognitive decline. METHODS Participants underwent annual testing autopsy. HNL, ADNC, LATE‐NC, other pathologies were evaluated. Regression mixed‐effects models examined association HNL with ADNC separately Path analyses extent to which associations LATE‐NC decline attributable HNL. RESULTS was associated more severe but only after excluding subjects sclerosis (HS). faster in global cognition episodic, semantic, working memory. In path analyses, about 61% whereas for it mostly independent DISCUSSION has an contribution acts as a major step LATE‐NC‐related Highlights Hippocampal (HNL) is prominent feature TDP‐43 (LATE‐NC) less so (ADNC). pathway LATE‐NC. Differential mechanisms degeneration are versus ADNC.

Language: Английский

Citations

1
Association between hippocampal microglia, AD and LATE‐NC, and cognitive decline in older adults DOI Creative Commons
Alifiya Kapasi, Lei Yu, Sue E. Leurgans

et al.

Alzheimer s & Dementia, Journal Year: 2024, Volume and Issue: 20(5), P. 3193 - 3202

Published: March 17, 2024

This study investigates the relationship between microglia inflammation in hippocampus, brain pathologies, and cognitive decline.

Language: Английский

Citations

3
Co-Aggregation of TDP-43 with Other Pathogenic Proteins and Their Co-Pathologies in Neurodegenerative Diseases DOI Open Access
Lei‐Lei Jiang,

Xiangle Zhang,

Hongyu Hu

et al.

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(22), P. 12380 - 12380

Published: Nov. 18, 2024

Pathological aggregation of a specific protein into insoluble aggregates is common hallmark various neurodegenerative diseases (NDDs). In the earlier literature, each NDD characterized by one or two pathogenic proteins, which can serve as disease-specific biomarkers. The these proteins thought to be major cause deleterious result in most NDDs. However, accumulating evidence shows that interact and co-aggregate with other different NDDs, thereby contributing disease onset progression synergistically. During past years, more than type has been found co-exist some individuals, may increase complexity pathogenicity diseases. This article reviews discusses biochemical characteristics molecular mechanisms underlying co-aggregation co-pathologies associated TDP-43 pathology. aggregates, amyotrophic lateral sclerosis (ALS) frontotemporal lobar degeneration (FTLD), often detected such Alzheimer's (AD), Parkinson's (PD), Huntington's (HD) spinocerebellar ataxia 2 (SCA2). many cases, shown multiple vitro vivo. Furthermore, co-occurrence have important consequences aggravate Thus, current viewpoint NDDs their relevance gain insights patho-mechanisms therapeutic potential

Language: Английский

Citations

0