Alzheimer's disease is a neurodegenerative disease that causes dementia. The pathological hallmarks of the disease are substantial neuronal cell loss, amyloid plaques consisting of amyloid peptide and intracellular neurofibrillary tangles containing hyperphosphorylated tau. Further, post-mortem analyses have ...
Alzheimer's disease is a neurodegenerative disease that causes dementia. The pathological hallmarks of the disease are substantial neuronal cell loss, amyloid plaques consisting of amyloid peptide and intracellular neurofibrillary tangles containing hyperphosphorylated tau. Further, post-mortem analyses have established that synapse loss precedes neuronal cell loss and correlates best with impaired memory. It is thought that soluble oligomeric amyloid peptides induce aberrant signalling that impairs synaptic function and neuronal survival. This aberrant singalling includes hyperphosphorylation of the cytoskeletal protein tau, a prerequisite for tangle formation. This indicates that protein kinases are dysregulated in Alzheimer's disease. Recently, a number of kinase dysregulations have been considered to occur in Alzheimer's disease. Since understanding of these kinase dysregulations could be a critical step for preventing neurodegeneration, we would like to discuss this research topic in detail.
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