Abstract
Alzheimer's disease is a chronic neurodegenerative disorder characterized by neuronal loss, cerebrovascular inflammation, and accumulation of senile plaques in the brain parenchyma and cerebral blood vessels. Amyloid-β peptide (Aβ), a major component of senile plaques, has been shown to exert multiple toxic effects to neurons, astrocytes, glial cells, and brain endothelium. Oligomeric Aβ can disturb the structure and function of cell membranes and alter membrane mechanical properties, such as membrane fluidity and molecular order. Much of these effects are attributed to their capability to trigger oxidative stress and inflammation. In this review, we discuss the effects of Aβ on neuronal cells, astrocytes, and cerebral endothelial cells with special emphasis on cell membrane properties and cell functions.
| Original language | English |
|---|---|
| Pages (from-to) | 138-148 |
| Number of pages | 11 |
| Journal | Molecular Neurobiology |
| Volume | 41 |
| Issue number | 2-3 |
| DOIs | |
| Publication status | Published - 2010 |
| Externally published | Yes |
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Keywords
- Alzheimer's disease
- Amyloid-β
- Cerebral endothelium
- Membrane fluidity
- Membrane order
- Membrane potential
- Membrane properties
ASJC Scopus subject areas
- Cellular and Molecular Neuroscience
- Medicine(all)
Cite this
Membrane biophysics and mechanics in alzheimer's disease. / Yang, Xiaoguang; Askarova, Sholpan; Lee, James C M.
In: Molecular Neurobiology, Vol. 41, No. 2-3, 2010, p. 138-148.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Membrane biophysics and mechanics in alzheimer's disease
AU - Yang, Xiaoguang
AU - Askarova, Sholpan
AU - Lee, James C M
PY - 2010
Y1 - 2010
N2 - Alzheimer's disease is a chronic neurodegenerative disorder characterized by neuronal loss, cerebrovascular inflammation, and accumulation of senile plaques in the brain parenchyma and cerebral blood vessels. Amyloid-β peptide (Aβ), a major component of senile plaques, has been shown to exert multiple toxic effects to neurons, astrocytes, glial cells, and brain endothelium. Oligomeric Aβ can disturb the structure and function of cell membranes and alter membrane mechanical properties, such as membrane fluidity and molecular order. Much of these effects are attributed to their capability to trigger oxidative stress and inflammation. In this review, we discuss the effects of Aβ on neuronal cells, astrocytes, and cerebral endothelial cells with special emphasis on cell membrane properties and cell functions.
AB - Alzheimer's disease is a chronic neurodegenerative disorder characterized by neuronal loss, cerebrovascular inflammation, and accumulation of senile plaques in the brain parenchyma and cerebral blood vessels. Amyloid-β peptide (Aβ), a major component of senile plaques, has been shown to exert multiple toxic effects to neurons, astrocytes, glial cells, and brain endothelium. Oligomeric Aβ can disturb the structure and function of cell membranes and alter membrane mechanical properties, such as membrane fluidity and molecular order. Much of these effects are attributed to their capability to trigger oxidative stress and inflammation. In this review, we discuss the effects of Aβ on neuronal cells, astrocytes, and cerebral endothelial cells with special emphasis on cell membrane properties and cell functions.
KW - Alzheimer's disease
KW - Amyloid-β
KW - Cerebral endothelium
KW - Membrane fluidity
KW - Membrane order
KW - Membrane potential
KW - Membrane properties
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U2 - 10.1007/s12035-010-8121-9
DO - 10.1007/s12035-010-8121-9
M3 - Article
VL - 41
SP - 138
EP - 148
JO - Molecular Neurobiology
JF - Molecular Neurobiology
SN - 0893-7648
IS - 2-3
ER -