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Hippocampal plasticity in Alzheimer's disease
M Mikkonen1, H Soininen, I Alafuzof
1Department of Neuroscience and Neurology, University Hospital and University of Kuopio, Finland.
Reviews in the Neurosciences
|January 11, 2002
Summary
Alzheimer's disease (AD) brains show structural plasticity changes, possibly as a response to damage or part of the disease process. Findings on PSA-NCAM and calcium-binding proteins support plasticity being integral to AD.
Area of Science:
- Neuroscience
- Pathology
- Cell Biology
Background:
- Alzheimer's disease (AD) is characterized by progressive neuropathology.
- Recent evidence suggests plasticity-related changes occur in the AD brain.
- These changes may represent compensatory mechanisms or be part of the disease cascade.
Purpose of the Study:
- To investigate the role of structural plasticity in Alzheimer's disease.
- To examine findings on polysialylated neural cell adhesion molecule (PSA-NCAM) and neuronal-expressed calcium-binding proteins in AD.
- To relate these findings to the broader understanding of plasticity in AD pathogenesis.
Main Methods:
- Analysis of the hippocampus and entorhinal cortex from control and AD patient brains.
- Investigation of highly polysialylated neural cell adhesion molecule (PSA-NCAM) expression.
- Assessment of neuronal-expressed calcium-binding proteins.
Main Results:
- Specific findings regarding PSA-NCAM and calcium-binding proteins in AD brains are discussed.
- These molecular changes are considered in the context of observed structural plasticity.
- The results suggest a significant role for plasticity in the AD disease process.
Conclusions:
- Structural plasticity is an integral component of Alzheimer's disease.
- Changes in molecules like PSA-NCAM and calcium-binding proteins are linked to plasticity in AD.
- Further research is warranted to fully elucidate the mechanisms and implications of plasticity in AD.