Molecular mechanisms of neuropathological changes in Alzheimer’s disease: a review

Abstract

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Letter to Editors Iron-induced fibrin formation may explain vascular pathology in Alzheimer’s disease

“…This concept is supported by the findings of Strickland and his group, who have shown that persistent fibrin deposits contribute to neuro-inflammation [3]. In conclusion, we believe that the information presented above supports arguments presented by Serý et al [6] that deserve further attention.…”

“…In their review article Serý et al [6] have presented compelling arguments in favour of the role of vascular mechanisms in the development of Alzheimer's disease (AD). These arguments are in line with a recent series of publications questioning the prevailing concept of amyloid beta-induced neurodegeneration.…”

Original article Mutations in the exon 7 of Trp53 gene and the level of p53 protein in double transgenic mouse model of Alzheimer’s disease

“…Alzheimer's disease (AD) is characterized both clinically by the decline of cognitive functions, such as memory, and pathologically by the presence of numerous senile plaques (SPs) and neurofibrillary tangles (NFTs) [2,3,28,40,46,51]. Neurofibrillary tangles consist of hyperphosphorylated tau protein, whereas Folia Neuropathologica 2014; 52/1 Trp53 and p53 in PS/APP mice SPs are composed of amyloid β-protein (Aβ).…”

Frontotemporal lobar degeneration with MAPT mutation in an Italian-Polish family. A

“…In addition, the increased inclusion of exon 10 in transcripts show an imbalance in the 3R and 4R tau isoforms [2,9,15]. The ratio of these two isoforms in normal condi tions is generally equal (1 : 1), but it varies depend ing on the type of mutation [24]. Corticobasal degen eration (CBD) is characterized by increased 4R tau, whereas frontotemporal lobar degeneration with Pick bodies shares an overabundance of 3R tau (Fig.…”