AI Article Synopsis
- Alzheimer's disease (AD) is characterized by synaptic and neuronal degeneration and the buildup of amyloid-beta (Abeta) in the brain, especially in areas associated with memory.
- While amyloid-beta can be found in healthy aging brains, its accumulation is seen as a key early event in the onset of Alzheimer's disease.
- The paper explores the normal functions of amyloid-beta and its precursor protein, AbetaPP, in brain development, particularly regarding how these roles could turn harmful as the brain ages.
Article Abstract
Pathological hallmarks of Alzheimer's disease (AD) include synaptic and neuronal degeneration and the presence of extracellular deposits of amyloid-beta (Abeta) in senile plaques in the cerebral cortex. Although these brain lesions may be seen also in aged non-demented individuals, the increase in brain Abeta is believed by many to represent the earliest event in the disease process. Accumulating evidence suggests that Abeta, which is highly conserved by evolution, may have an important physiological role in synapse elimination during brain development. An intriguing idea is that this putative function can become pathogenic if activated in the aging brain. Here, we review the literature on the possible physiological roles of Abeta and its precursor protein AbetaPP during development with special focus on electrophysiological findings.
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| http://dx.doi.org/10.3233/JAD-2009-0918 | DOI Listing |
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