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Davidson et al. Acta Neuropathologica Communications (2018) six:56 https://doi.org/10.1186/s40478-018-0559-RESEARCHOpen AccessThe age of onset and evolution of Braak tangle stage and Thal amyloid pathology of Alzheimer’s disease in people with Down syndromeYvonne S. Davidson1, Andrew Robinson1, Vee P. Prasher2,3 and David M. A. Mann1*AbstractWhile post mortem research have identified the significant cell sorts and functional systems impacted in Alzheimer’s disease (AD) the initial web pages and molecular characteristics of pathology are nevertheless unclear. Because people with Down syndrome (DS) (trisomy 21) develop the full pathological changes of AD inside a predictable way by the time they reach middle to late age, a study of your brains of such persons at various ages tends to make a perfect `model system’ in which the web-sites of earliest onset of pathology is usually detected and the subsequent progression of modifications be monitored. Inside the present study we’ve got examined the brains of 56 men and women with DS ranging from new-born to 76 years for the presence of amyloid and tau pathology in key cortical and BCMA/TNFRSF17 Protein Human subcortical regions. Amyloid pathology was found to commence within the late teens to twenties as a deposition of diffuse plaques initially inside the temporal neocortex, rapidly involving other neocortical regions but only reaching subcortical regions and cerebellum by the late forties. Cerebral amyloid angiopathy didn’t regularly commence till immediately after 450 years of age. Tau pathology generally commenced soon after 35 years of age, initially involving not merely entorhinal locations and hippocampus but additionally subcortical regions like locus caeruleus (LC) and dorsal raphe nucleus (DRN). Later, tau pathology spread throughout the neocortex reaching occipital lobes in most instances by mid-50 years of age. Such a pattern of spread is constant with that seen in typical AD. We discovered no evidence that tau pathology may possibly commence within the brain in DS ahead of amyloid deposition had occurred, but there was limited data that suggests tau pathology in LC or DRN could predate that in entorhinal locations and hippocampus or at the very least be coincident. Keyword phrases: Alzheimer’s disease, Down syndrome, Amyloid, TauIntroduction Alzheimer’s disease (AD) is characterised pathologically by the abundant presence of deposits of amyloid protein (A) inside the brain parenchyma inside the form of amyloid plaques, and in blood vessel walls as cerebral amyloid angiopathy (CAA), and neurofibrillary tangles (NFT) composed of hyperphosphorylated tau proteins [19, 35]. Even though post mortem studies based on established circumstances of AD have identified the major cell forms and functional systems impacted by the disorder, the initial websites of pathology are* Correspondence: [email protected] 1 Institute of Brain, Behaviour and Mental Wellness, Faculty of Medical and Human Sciences University of Manchester, Salford Royal Hospital, Stott Lane, Salford M6 8HD, England Full list of author facts is accessible in the end with the articlestill unclear. Accordin.