@entity195 appears to be a stereotyped mode of reaction of the central nervous system to various types of aggression such as different mutations involving various proteins, trisomy 21 or repeated @entity542 as in @entity303 . Rather than a disease, it appears to be a clinicopathological syndrome due to various causes. Lesions may be considered under 3 headings: neurofibrillary pathology, @entity477 peptide deposits and loss (neuronal and synaptic). Neurofibrillary pathology includes the @entity3072 , the crown of the @entity527 and the neuropil threads. All those lesions are characterized by the same ultrastructure--i.e. the accumulation of paired helical filaments--and the same immunohistochemistry: they are labelled by antibodies directed against the tau proteins. The @entity527 , present in the core of the @entity527 and in the vascular walls, are made of a 40 to 42 @entity1522 long peptide, named @entity477 , derived from the @entity477 ( @entity477 ). Antibodies directed against the @entity477 peptide also label diffuse deposits that are devoid of the tinctorial affinities and of the biochemical properties of amyloid substances. Those diffuse deposits are insufficient to cause @entity303 since they may be observed in high density in aged @entity1 without intellectual deterioration. @entity528 occurs after neurofibrillary pathology. The role of the synaptic pathology remains discussed. Besides tau proteins, @entity477 peptide and @entity477 , several other proteins may play an important role: @entity2204 which could act as a chaperone protein, inducing or facilitating the formation of amyloid, @entity68642 , mutated in some cases of @entity195 , @entity8095 which is present in the @entity1832 found in @entity191 and in @entity303 with @entity1832 . The @entity477 deposits are diffusely distributed in the cerebral cortex; the neurofibrillary changes have a hierarchical distribution. The progression of the neurofibrillary pathology in the various cortical areas follow a stereotyped sequence that may help to grade the severity of the disease. Progression may take decades. The relations between aging and @entity195 are still poorly understood. Frequency of @entity195 in old @entity1 could suggest that they are the inevitable burden of age, but this has been discussed.

[ XXXX : lesions and their progression].

@entity1 :: ('9606', 'Species') :: ['people'] @entity1522 :: ('CHEBI:33709', 'Chemical') :: ['amino-acids'] @entity68642 :: ('5663;5664', 'Gene') :: ['presenilins 1 and 2'] @entity527 :: ('MESH:D058225', 'Disease') :: ['amyloid deposits', 'senile plaque'] @entity8095 :: ('6622', 'Gene') :: ['alpha-synuclein'] @entity2204 :: ('348', 'Gene') :: ['apolipoprotein E'] @entity303 :: ('MESH:D003704', 'Disease') :: ['dementia pugilistica', 'dementia'] @entity542 :: ('MESH:D006259', 'Disease') :: ['head trauma'] @entity3072 :: ('MESH:C536599', 'Disease') :: ['neurofibrillary tangle'] @entity191 :: ('MESH:D010300', 'Disease') :: ['Parkinson disease'] @entity477 :: ('351', 'Gene') :: ['APP', 'amyloid precursor protein', 'A beta'] @entity1832 :: ('MESH:D020961', 'Disease') :: ['Lewy bodies'] @entity195 :: ('MESH:D000544', 'Disease') :: ['familial Alzheimer disease', 'Alzheimer type lesions', 'Alzheimer disease'] @entity528 :: ('MESH:D009410', 'Disease') :: ['Neuronal loss']
@entity195 :: (MESH:D000544,Disease) :: ['Alzheimer's disease']
