Endoplasmic reticulum stress and prion diseases
-
Kun Xu
and
Xiu-Ping Zhu
Abstract
The endoplasmic reticulum (ER), an important cellular organelle in eukaryotic cells, becomes dysfunctional following exposure to harmful stimuli. These stimuli can cause the ER stress response, which induces cell apoptosis due to changes in ER protein levels such as glucose-regulated protein. Current studies indicate that ER stress is closely related to the occurrence and development of neurodegenerative disorders, e.g., prion diseases. The pathogenic agent known as the misfolded prion protein may cause an imbalance in ER homeostasis and commit the neuron to a pathway of apoptosis; however, the specific mechanisms are still under intensive investigation. This review summarizes current research investigating the relationship between ER stress and prion diseases. These findings will aid in the development of novel strategies for diagnosis and therapies for prion and other neurodegenerative diseases.
©2012 by Walter de Gruyter Berlin Boston
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Articles in the same Issue
- GSK3: a key target for the development of novel treatments for type 2 diabetes mellitus and Alzheimer disease
- Mitochondrial and metabolic-based protective strategies in Huntington’s disease: the case of creatine and coenzyme Q
- At a PI3K crossroads: lessons from flies and rodents
- Theta phase precession beyond the hippocampus
- The role of Ca2+-stimulated adenylyl cyclases in bidirectional synaptic plasticity and brain function
- Endoplasmic reticulum stress and prion diseases
- Head models and dynamic causal modeling of subcortical activity using magnetoencephalographic/electroencephalographic data
- The role of glutamatergic inputs onto parvalbumin-positive interneurons: relevance for schizophrenia
- Stress-linked cortisol concentrations in hair: what we know and what we need to know
- Prelims
- Prelims
