@entity195 , the cause of one of the most common types of @entity303 , is a @entity75 affecting the elderly and is characterized by the formation of two main protein aggregates: senile plaques and @entity3072 , which are involved in the process leading to progressive @entity528 and @entity204 . Neurodegeneration in @entity195 is a pathologic condition of cells rather than an accelerated way of aging. The senile plaques are generated by a deposition in the @entity1 brain of fibrils of the @entity477 (Abeta), a fragment derived from the proteolytic processing of the amyloid precursor protein (APP). Tau protein is the major component of paired helical filaments (PHFs), which form a compact filamentous network described as @entity3072 ( @entity3072 ). Experiments with hippocampal cells in culture have indicated a relationship between fibrillary amyloid and the cascade of molecular signals that trigger tau hyperphosphorylations. Two main protein kinases have been shown to be involved in anomalous tau phosphorylations: the cyclin-dependent kinase @entity22445 and glycogen synthase kinase @entity9459 . @entity22445 plays a critical role in brain development and is associated with neurogenesis as revealed by studies in brain cells in culture and @entity521 cells. Deregulation of this protein kinase as induced by extracellular amyloid loading results in tau hyperphosphorylations, thus triggering a sequence of molecular events that lead to @entity528 . Inhibitors of @entity22445 and @entity9459 and antisense oligonucleotides exert protection against @entity528 . On the other hand, there is cumulative evidence from studies in cultured brain cells and on brains that oxidative stress constitutes a main factor in the modification of normal signaling pathways in neuronal cells, leading to biochemical and structural @entity179 as related to the pathogenesis of @entity195 . This review is focused on the main protein aggregates responsible for @entity528 in both sporadic and familial forms of @entity195 , as well as on the alterations in the normal signaling pathways of functional neurons directly involved in @entity179 . The analysis is extended to the action of neuroprotective factors including selective inhibitors of tau phosphorylating protein kinases, @entity172 , and antioxidants among other molecules that apparently prevent @entity528 .

The molecular bases of XXXX and other @entity179 .

@entity1 :: ('9606', 'Species') :: ['human'] @entity172 :: ('MESH:D004967', 'Chemical') :: ['estrogens'] @entity303 :: ('MESH:D003704', 'Disease') :: ['dementia'] @entity75 :: ('MESH:D001927', 'Disease') :: ['brain disorder'] @entity3072 :: ('MESH:C536599', 'Disease') :: ['NFTs', 'neurofibrillary tangles'] @entity477 :: ('351', 'Gene') :: ['beta-amyloid peptide'] @entity22445 :: ('1020', 'Gene') :: ['Cdk5'] @entity179 :: ('MESH:D019636', 'Disease') :: ['neurodegeneration', 'abnormalities and neurodegeneration'] @entity521 :: ('MESH:D009447', 'Disease') :: ['neuroblastoma'] @entity195 :: ('MESH:D000544', 'Disease') :: ["Alzheimer's disease"] @entity204 :: ('MESH:D003643', 'Disease') :: ['death'] @entity9459 :: ('2932', 'Gene') :: ['GSK3beta'] @entity528 :: ('MESH:D009410', 'Disease') :: ['neuronal death', 'neuronal degeneration']
@entity195 :: (MESH:D000544,Disease) :: ['Alzheimer's disease']
