Year: 2005
Type: review
Abstract: Sporadic Alzheimer's disease is the leading cause of dementia, but the underlying molecular processes are still unknown. Several studies have observed an accumulation of the protein fragment p25 in sporadic Alzheimer's disease brain. p25 derives from proteolysis of p35, and overactivates the tau kinase cyclin-dependent kinase 5. Transgenic mice expressing high levels of p25 exhibit hyperphosphorylation of tau as seen in Alzheimer's disease, and neurodegeneration. In contrast, low-level p25 expression, less than half of endogenous p35 expression, has a sex-specific effect on hippocampal synaptic plasticity and improves spatial learning in female but not in male mice. Therefore, p25 formation may initially be a compensatory response for early learning deficits in Alzheimer's disease, but continued formation could contribute to detrimental changes in Alzheimer's disease.
Source: Neuroreport
Authors: K. Peter Giese, Laurence Ris, Florian Plattner
Institutions: University College London, University of Mons
Language: English
Subfield: Cellular and Molecular Neuroscience
Field: Neuroscience
Domain: Life Sciences
Open Access status: green
OpenAlex ID: W2169035195