The Relationship of Microglial Cells to Dying Neurons During Natural Neuronal Cell Death and Axotomy-induced Degeneration of the Rat Retina

1991 ◽  
Vol 3 (12) ◽  
pp. 1189-1207 ◽  
Author(s):  
Solon Thanos
Nitric Oxide ◽  
2010 ◽  
Vol 22 (1) ◽  
pp. 18-29 ◽  
Author(s):  
Gyu Hwan Park ◽  
Se Jin Jeon ◽  
Hyun Myung Ko ◽  
Jae Ryun Ryu ◽  
Jong Min Lee ◽  
...  

2020 ◽  
Vol 14 ◽  
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Mayumi Asada ◽  
Hideki Hayashi ◽  
Kenjiro Murakami ◽  
Kento Kikuiri ◽  
Ryotaro Kaneko ◽  
...  

2017 ◽  
Vol 7 (1) ◽  
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Claudio Bussi ◽  
Javier Maria Peralta Ramos ◽  
Daniela S. Arroyo ◽  
Emilia A. Gaviglio ◽  
Jose Ignacio Gallea ◽  
...  

2010 ◽  
Vol 635 (1-3) ◽  
pp. 56-61 ◽  
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Kenji Sakamoto ◽  
Masahide Hiraiwa ◽  
Maki Saito ◽  
Tsutomu Nakahara ◽  
Yoji Sato ◽  
...  

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Zhenzhen Liu ◽  
Tao Li ◽  
Ping Li ◽  
Nannan Wei ◽  
Zhiquan Zhao ◽  
...  

Alzheimer’s disease (AD) is the most common form of dementia. The pathological hallmarks of AD are amyloid plaques [aggregates of amyloid-beta (Aβ)] and neurofibrillary tangles (aggregates of tau). Growing evidence suggests that tau accumulation is pathologically more relevant to the development of neurodegeneration and cognitive decline in AD patients than Aβplaques. Oxidative stress is a prominent early event in the pathogenesis of AD and is therefore believed to contribute to tau hyperphosphorylation. Several studies have shown that the autophagic pathway in neurons is important under physiological and pathological conditions. Therefore, this pathway plays a crucial role for the degradation of endogenous soluble tau. However, the relationship between oxidative stress, tau protein hyperphosphorylation, autophagy dysregulation, and neuronal cell death in AD remains unclear. Here, we review the latest progress in AD, with a special emphasis on oxidative stress, tau hyperphosphorylation, and autophagy. We also discuss the relationship of these three factors in AD.


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