scholarly journals Proteomic analysis of human hippocampal subfields provides new insights into the pathogenesis of Alzheimer’s disease and the role of glial cells

2022 ◽  
Author(s):  
Yanpan Gao ◽  
Jiaqi Liu ◽  
Jiayu Wang ◽  
Yifan Liu ◽  
Ling‐Hui Zeng ◽  
...  
2017 ◽  
Vol 13 (7S_Part_16) ◽  
pp. P788-P789
Author(s):  
Marzia Antonella Scelsi ◽  
Eugenio Iglesias ◽  
Jonathan M. Schott ◽  
Sebastien Ourselin ◽  
Andre Altmann ◽  
...  

2017 ◽  
Vol 13 (7S_Part_1) ◽  
pp. P40-P41 ◽  
Author(s):  
Marzia Antonella Scelsi ◽  
Eugenio Iglesias ◽  
Jonathan M. Schott ◽  
Sebastien Ourselin ◽  
Andre Altmann ◽  
...  

Biomolecules ◽  
2018 ◽  
Vol 8 (3) ◽  
pp. 93 ◽  
Author(s):  
Saif Nirzhor ◽  
Rubayat Khan ◽  
Sharmind Neelotpol

Even though Alzheimer’s disease (AD) is of significant interest to the scientific community, its pathogenesis is very complicated and not well-understood. A great deal of progress has been made in AD research recently and with the advent of these new insights more therapeutic benefits may be identified that could help patients around the world. Much of the research in AD thus far has been very neuron-oriented; however, recent studies suggest that glial cells, i.e., microglia, astrocytes, oligodendrocytes, and oligodendrocyte progenitor cells (NG2 glia), are linked to the pathogenesis of AD and may offer several potential therapeutic targets against AD. In addition to a number of other functions, glial cells are responsible for maintaining homeostasis (i.e., concentration of ions, neurotransmitters, etc.) within the central nervous system (CNS) and are crucial to the structural integrity of neurons. This review explores the: (i) role of glial cells in AD pathogenesis; (ii) complex functionalities of the components involved; and (iii) potential therapeutic targets that could eventually lead to a better quality of life for AD patients.


2016 ◽  
Vol 13 (1) ◽  
Author(s):  
David Heras-Sandoval ◽  
José Pedraza-Chaverri ◽  
Jazmin M. Pérez-Rojas

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Celia Luchena ◽  
Jone Zuazo-Ibarra ◽  
Elena Alberdi ◽  
Carlos Matute ◽  
Estibaliz Capetillo-Zarate

Synapse loss is an early manifestation of pathology in Alzheimer’s disease (AD) and is currently the best correlate to cognitive decline. Microglial cells are involved in synapse pruning during development via the complement pathway. Moreover, recent evidence points towards a key role played by glial cells in synapse loss during AD. However, further contribution of glial cells and the role of neurons to synapse pathology in AD remain not well understood. This review is aimed at comprehensively reporting the source and/or cellular localization in the CNS—in microglia, astrocytes, or neurons—of the triggering components (C1q, C3) of the classical complement pathway involved in synapse pruning in development, adulthood, and AD.


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