Braak staging

Braak staging

A system formulated in 1991 by Drs. Braak and Braak (Acta Neuropathologica Berl—82:239-259) for staging the severity of Alzheimer’s disease (AD), based on the premise that AD pathology—specifically neurofibrillary tangles—evolve in stages and locations, beginning in the mesial temporal lobe (stages 1 and 2) and extending to the limbic regions (stages 3 and 4)—at which point dementia manifests itself clinically—ending in the neocortex (stages 5 and 6).
References in periodicals archive ?
Braak staging of Parkinson's disease is based on pathological findings.
Progressive pathological tau severity (Braak staging) has been characterized based on postmortem autopsies by Braak and Braak.[58] Neurofibrillary pathology initiates within the anteromedial temporal lobe, progressing to the hippocampus proper and multimodal association areas, eventually spreading to secondary and primary cortices.
Elevations in A[sz] corresponded to the spreading of tau pathology to the lateral temporal lobe and neocortex, accurately correlating with changes in cognition during normal aging, and transitional phases from MCI to AD.[115] This highlights the value of tau tracers during in vivo Braak staging and suggests that tau pathology in regions beyond the medial temporal lobe may be strong indicators for advanced AD onset.
Sliwinski et al., "Memory and mental status correlates of modified Braak staging," Neurobiology of Aging, vol.
"This was consistent with Braak stage V/VI, which was confirmed by our in vivo Braak staging," they added.
(2009) found that MRI diagnosis of medial-temporal lobe atrophy, when matched to postmortem neuropathological data (Braak staging and quantitative analysis of amyloid-[beta] plaque, tau tangle and Lewy body load), resulted in 91% sensitivity and 94% specificity in distinguishing between DLB, AD, and vascular cognitive impairment.
A critical evaluation of the Braak staging scheme for Parkinson's disease.
(5) The main criticism of this system is that it fails to adequately address the significance of neurofibrillary tangles, which in many studies correlate better with clinically identified dementia.8 In contrast, Braak staging correlates well with clinical dementia but does not adequately address the contribution of amyloid/plaque pathology to some cases of AD, particularly familial forms.
Braak staging of neurofibrillary spread was also performed.
For example, while Braak staging is the gold standard from a clinical standpoint, it is rarely applicable in animal models because tau transgenes are typically driven by ubiquitous promoters that express tau in all neurons simultaneously.
Braak staging of the three groups was, respectively, Con: 1.4 [+ or -] 0.2, Dem: 1.5 [+ or -] 0.2, and AD: 4.8 [+ or -] 0.3.
The clinicopathological data of the patients and the Braak staging for PD and AD of all donors is summarized in Table 1.