Cerebellar involvement is variable, but can often be severe [6]

Cerebellar involvement is variable, but can often be severe [6]. The reasons for this differential brain vulnerability to CAA remain obscure, but might relate

to varying efficiencies in perivascular drainage of parenchymally derived Aβ associated with Alzheimer-type pathology, given the observations that (in AD) the occipital cortex (where CAA is usually most severe) is often little affected by SP, and is always the least/last to be affected by tau pathology [7]. Because of the emphasis placed on the pathological staging systems for NFT [6], neuritic plaques [8] and Aβ [9], AD is largely thought of as a fairly ‘uniform’ and ‘predictable’ entity, passing through various hierarchical stages in the course of its evolution. However, subtle neuropsychological DAPT order assessment reveals a clinically heterogeneous picture, especially in early stages of the disease where distinct memory, language, visual and frontal predominant syndromes can be seen [10]. There are also heterogeneities in the extent and distribution of the

main histopathological changes, particularly in relationship to CAA [11]. The present study sought to investigate a series of cases of AD with respect to the extent, distribution and morphological appearance of the neocortical deposition of Aβ as SP and CAA. Four histological phenotypes were discerned, and comparisons of their clinical, demographic and genetic features were performed. One hundred and thirty-four cases of AD were investigated. There were 67 men and 67

women. The age of onset ranged from 35 to 89 years (mean = 64.5 ± 11.0 MAPK inhibitor years), age of death ranged from 45 to 97 years (mean = 73.8 ± 10.2 years), and the duration of illness from 1 to 19 years (mean = 8.1 ± 3.0 years). Brain weight ranged from 760 g to 1456 g (mean = 1137 ± 154 g). The presence of previous family history or not had been documented in 120 patients, although this was definitely positive Flavopiridol (Alvocidib) in only 14. Genetic analyses (other than APOE genotyping) had not been performed for any case. Pathological diagnoses were made by an experienced neuropathologist (D.M.A.M.), and were in accordance with recent National Institute on Ageing – Alzheimer’s Association guidelines for the neuropathological assessment of Alzheimer’s disease [12]. Based on investigations of representative areas of frontal, temporal and parietal cortical regions, all cases had Consortium to Establish a Registry for Alzheimer’s Disease (CERAD) score of C for neuritic plaques [8] and were at Braak stage V or VI for neurofibrillary changes [7]. All cases were obtained from the Manchester Brain Bank through appropriate consenting procedures for the collection and use of the human brain tissues. The clinical phenotype, as defined by Stopford et al. [10], was available for 52 of the 134 cases.

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