Stages of the Pathologic Process in Alzheimer Disease: Age Categories From 1 to 100 Years

By H. Braak, D. Thal, E. Ghebremedhin, K. Del Tredici. Journal of Neuropathology and Experimental Neurology, 2011

1,949 citations recorded by the source corpus.

Subfields: Neurology, Physiology, Psychiatry and Mental health

View Paper: https://www.semanticscholar.org/paper/304114ea8f7ae29d50bad22e6d1546a9be3e1855

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Citations in the corpus

A/T/N: An unbiased descriptive classification scheme for Alzheimer disease biomarkers (2016, background): “Tauopathy confined to the medial temporal lobes with minimal or no neocortical b-amyloidosis is very common at autopsy and whether this should be regarded as AD or simply an aging phenomenon is controversial.(12,13,44) One possible approach to categorizing tau PET is to label scans that have tracer ”
PET Imaging of Tau Deposition in the Aging Human Brain (2016, neutral): “Further, by characterizing participants according to Braak stage, we also found, consistent with previous findings (Braak and Braak, 1991, 1997; Braak et al., 2006, 2011; Nelson et al., 2012; Serrano-Pozo et al., 2011), increasing Braak stage in cognitively healthy and diseased participants to be…”
National Institute on Aging–Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease (2012, neutral): “NFTs commonly are observed in limbic regions early in the disease but, depending on disease stage, also involve other brain regions, including association cortex, some subcortical nuclei, and even some brainstem regions [28], where their formation may precede that in limbic structures [29].”
Pathology of Neurodegenerative Diseases. (2017, background): “A recent revision of this scheme suggests that tau pathology in subcortical areas, such as the locus coeruleus in the pons, may precede medial temporal lobe pathology (Braak et al. 2011).”
Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature (2012, background): “At 40 years, all individuals studied by Braak and Del Tredici (39) and Braak et al (44) exhibited at least initial neuroﬁbrillary pathology in the brain-stem (Fig.”
Primary age-related tauopathy (PART): a common pathology associated with human aging (2014, methodology): “The rationale for including extracortical tau pathology in PART is that the pathologies commonly coexist and that brain-stem NFTs, if they represent the same process, appear to occur even earlier in human aging [30–32 , 53 ].”
Stages of pTDP‐43 pathology in amyotrophic lateral sclerosis (2013, methodology): “The first set was stained with aldehyde fuchsin–Darrow red for topographical orientation and evaluation of neuronal loss (lipofuscin pigment deposits, basophilic Nissl material).(4,6) pTDP-43 pathology was analyzed in the second set using a commercially available 409=410 rabbit polyclonal antibody (”
Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models (2014, background): “Second, it appears that density of neuritic plaques correlates more strongly with the cognitive deﬁcits than do “diffuse” amyloid plaques (Mckee et al., 1991; Crystal et al., 1993; Tiraboschi et al., 2004; Nelson et al., 2007a; Braak et al., 2011).”
Predicting regional neurodegeneration from the healthy brain functional connectome. (2012, background): “Regions showing greatest atrophy at later stages may or may not represent the sites of initial injury, and even longitudinal imaging studies that follow patients from health to disease may overlook incipient microscopic pathology within small neuronal populations (Braak et al., 2011).”
Physiological release of endogenous tau is stimulated by neuronal activity (2013, neutral): “In Alzheimer’s disease and related disorders, characteristic neuropathological depositions of the cytoskeletal protein tau spread progressively from the entorhinal cortex to anatomically connected brain regions [1,2].”