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Neuropathological Features of Aging and Neurodegenerative Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: 31 July 2024 | Viewed by 733

Special Issue Editor


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Guest Editor
The Jikei University School of Medicine, Tokyo, Japan
Interests: neuropathology; aging; Alzheimer’s disease; Parkinson’s disease; Parkinsonism; progressive supranuclear palsy; corticobasal degeneration

Special Issue Information

Dear Colleagues,

In recent years, the relationship between abnormal protein accumulation in neurons and aging has garnerd significant attention, particularly in the context of neurodegenerative diseases, such as Alzheimer’s disease and Parkinson’s disease. Understanding the changes in the brain and the aging process of neural tissues is a crucial step towards preventing and treating neurodegenerative disease, and Alzheimer’s disease (AD) and Parkinson’s disease (PD) constitute representative examples. Notably, the FDA’s approval of antibody therapy targeting amyloid beta in AD has sparked considerable interest. This milestone holds great significance in AD, a disease characterized by the presence of two types of abnormal protein accumulation: tau and amyloid. While antibody therapies for PD, primarily targeting alpha-synuclein, were anticipated, unfortunately, they were all prematurely halted during their clinical trials.

This Special Issue aims to focus on the association between aging and neurodegenerative disease while highlighting neuropathological features and presenting the latest research findings in this field. By comprehending the changes in the brain during aging, we will delve into the neuropathological characteristics of major neurodegenerative disease, such as AD, PD, PSP, and CBD. Moreover, we will provide an overview of the recent advancements in research related to abnormal proteins implicated in neurodegenerative diseases, including tau, amyloid beta, and alpha-synuclein. The potential for early diagnosis and treatment strategies based on neuropathological features will also be addressed. Through this refined collection of articles, we aim to shed light on the intricate connection between aging and neurodegenerative diseases, offering valuable findings for researchers, clinicians, and healthcare professionals, and fostering new perspectives in the understanding and management of neurodegenerative disorders.

Dr. Renpei Sengoku
Guest Editor

Manuscript Submission Information

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Keywords

  • neuropathology
  • aging
  • Alzheimer’s disease
  • Parkinson’s disease
  • Parkinsonism
  • progressive supranuclear palsy
  • cortcobasal degeneration

Published Papers (1 paper)

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10 pages, 934 KiB  
Case Report
Age-Related Pathology in Corticobasal Degeneration
by Maya Mimuro and Yasushi Iwasaki
Int. J. Mol. Sci. 2024, 25(5), 2740; https://doi.org/10.3390/ijms25052740 - 27 Feb 2024
Viewed by 521
Abstract
Elderly human brains are vulnerable to multiple proteinopathies, although each protein has a different transmission pathway. Tau-immunoreactive astrocytes are well-known in elderly brains. In contrast, astrocytic plaques, a hallmark in corticobasal degeneration (CBD), rarely occur in aging and neurodegenerative disease other than CBD. [...] Read more.
Elderly human brains are vulnerable to multiple proteinopathies, although each protein has a different transmission pathway. Tau-immunoreactive astrocytes are well-known in elderly brains. In contrast, astrocytic plaques, a hallmark in corticobasal degeneration (CBD), rarely occur in aging and neurodegenerative disease other than CBD. To elucidate the clinicopathological correlation of aging-related pathology in CBD, we examined 21 pathologically proven CBD cases in our institute (12 males and 9 females, with a mean age of death 70.6 years). All CBD cases showed grains and neurofibrillary tangles (NFTs). Fifteen cases (71.4%) showed beta-amyloid deposition such as senile plaques or cerebral amyloid angiopathy. Three cases (14.3%) had Lewy body pathology. One case was classified as amygdala-predominant Lewy body disease, although no cases met the pathological criteria for Alzheimer’s disease. Five cases (23.8%) displayed Limbic-predominant and age-related TDP-43 encephalopathy (LATE). NFTs, grains, and TDP-43-positive neuronal inclusions were widely distributed throughout the limbic system of CBD patients, but their densities were low. CBD might a have similar cell vulnerability and transmission pathway to that of multiple proteinopathy in aging brains. Full article
(This article belongs to the Special Issue Neuropathological Features of Aging and Neurodegenerative Diseases)
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Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

In recent years, the relationship between abnormal protein accumulation in neurons and aging has garnerd significant attention, particularly in the context of neurodegenerative diseases, such as Alzheimer’s disease and Parkinson’s disease. Understanding the changes in the brain and the aging process of neural tissues is a crucial step towards preventing and treating neurodegenerative disease, and Alzheimer’s disease (AD) and Parkinson’s disease (PD) constitute representative examples. Notably, the FDA’s approval of antibody therapy targeting amyloid beta in AD has sparked considerable interest. This milestone holds great significance in AD.

This Special Issue aims to focus on the association between aging and neurodegenerative disease while highlighting neuropathological features and presenting the latest research findings in this field. By comprehending the changes in the brain during aging, we will delve into the neuropathological characteristics of major neurodegenerative disease. Moreover, we will provide an overview of the recent advancements in research related to abnormal proteins implicated in neurodegenerative diseases, including tau, amyloid beta, and alpha-synuclein.

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