Apolipoprotein E and cognitive performance
Article Abstract:
Spatial memory is impaired in mice with the apolipoprotein (APO) E4 variant, which increases the risk of developing Alzheimer's disease compared with apoE3. However, spatial memory is not impaired in mice with apoE3, even though the levels of beta-amyloid in their brains are similar. It is clear that apoE3, but not apoE4, can protect against cognitive deficits prompted by beta-amyloid. This may be the reason why human apoE4 carriers are at higher risk of developing Alzheimer's than apoE3 carriers. The connection between apoE4 and the higher risk of developing Alzheimer's could be at least partly attributable to the differential capacity of apoE isoforms to prevent functional neuronal deficits prompted by A-beta or other human beta-amyloid precursor proteins.
Publication Name: Nature
Subject: Zoology and wildlife conservation
ISSN: 0028-0836
Year: 2000
User Contributions:
Comment about this article or add new information about this topic:
A network dysfunction perspective on neurodegenerative diseases
Article Abstract:
A reversible network dysfunction is a therapeutic entry point that can be useful in treating patients with Alzheimer's disease (AD) or other neurodegenerative disorders. Enhancing neuronal plasticity might help the remaining neural circuits to compensate for lost or broken circuits and improving network activity might help in preventing the inexorable less of neuronal processes and cellbodies that occurs in AD and other neurodegenerative diseases.
Publication Name: Nature
Subject: Zoology and wildlife conservation
ISSN: 0028-0836
Year: 2006
User Contributions:
Comment about this article or add new information about this topic:
Amyloidogenic role of cytokine TGF-beta1 in transgenic mice and in Alzheimer's disease
Article Abstract:
An important characteristic of Alzheimer's disease is the formation of amlyloid-beta plaques in the brain, which could be a possible cause of its degradation. A new study of transgenic mice shows that over-expression of TGF-beta1 induces amyloid deposition in cerebral blood vessels, correlating with increased levels of amyloid-beta1 deposition in the cerebral blood vessels of Alzheimer patients.
Publication Name: Nature
Subject: Zoology and wildlife conservation
ISSN: 0028-0836
Year: 1997
User Contributions:
Comment about this article or add new information about this topic:
- Abstracts: A pore way to die. Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases
- Abstracts: The age of the Amazon's breath. An earth-system perspective of the global nitrogen cycle. Anthropogenically enhanced fluxes of water and carbon from the Mississippi River
- Abstracts: A self-replicating peptide. A synthetic peptide ligase. Antibacterial agents based on the cyclic D,L-alpha-peptide architecture
- Abstracts: The PIE-1 protein and germline specification in C. elegans embryos. Exclusion of germ plasm proteins from somatic lineages by cullin-dependent degradation
- Abstracts: Nest and egg clutches of the dinosaur Troodon formosus and the evolution of avian reproductive traits. Parental care in an ornithischian dinosaur: A dramatic fossil may shed light on how modern archosaurs became devoted parents