Neuropathological stageing of Alzheimer-related changes

  title={Neuropathological stageing of Alzheimer-related changes},
  author={Heiko Braak and E. van Braak},
  journal={Acta Neuropathologica},
SummaryEighty-three brains obtained at autopsy from nondemented and demented individuals were examined for extracellular amyloid deposits and intraneuronal neurofibrillary changes. The distribution pattern and packing density of amyloid deposits turned out to be of limited significance for differentiation of neuropathological stages. Neurofibrillary changes occurred in the form of neuritic plaques, neurofibrillary tangles and neuropil threads. The distribution of neuritic plaques varied widely… 
Allocortical neurofibrillary changes in progressive supranuclear palsy
Silver techniques for intraneuronal cytoskeleton abnormalities and extracellular A4-amyloid deposits were used to examine lesions of the cerebral cortex in six cases of progressive supranuclear palsy and a characteristic pattern of changes was found in the entorhinal cortex.
A grading system of Alzheimer disease lesions in neocortical areas
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Although the role of plaques and NFT in the pathogenesis of AD remains undetermined, clinicopathological correlative studies have shown that both lesions, if present in sufficient numbers, particularly in the neocortex, are considered the best morphological signposts for AD.
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Early Alzheimer-type lesions in cognitively normal subjects
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The data suggest that tauopathy associated with sporadic Alzheimer disease may begin earlier than previously thought and possibly in the lower brainstem rather than in the transentorhinal region.
Cortical thinning of parahippocampal subregions in very early Alzheimer's disease
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The relationship between subcortical tau pathology and Alzheimer's disease.
These findings suggest that the LC becomes increasingly involved during AD progression rather than representing the site initially affected, and the severity of tau pathology in the LC significantly increases with increasing NFT Braak stages.
Neurofibrillary tangle predominant form of senile dementia of Alzheimer type: a rare subtype in very old subjects
This rare subtype occurring in very old (over 80 years of age) subjects that does not fall within the currently used neuropathological criteria for diagnosis of AD warrants further clinico-pathological documentation.


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Sensitive and specific silver methods were applied to examine the pathology revealed by the occipital isocortex in cases of Alzheimer's disease and age-matched controls to demonstrate amyloid and neurofibrillary changes are encountered in plaque-like formations.
Alzheimer's disease affects limbic nuclei of the thalamus
Sensitive silver techniques for amyloid and neurofibrillary changes were applied to examine the pathological changes revealed by limbic nuclei of the thalamus in Alzheimer's disease and showed the most severe involvement in the antero-dorsal nucleus.
Anatomical correlates of the distribution of the pathological changes in the neocortex in Alzheimer disease.
Data on the severity of the pathological involvement in different areas of the neocortex and the laminar distribution and the clustering of the tangles support the suggestion that the pathological changes in Alzheimer disease affect regions that are interconnected by well-defined groups of connections and that the disease process may extend along the connecting fibers.
Neurofibrillary changes confined to the entorhinal region and an abundance of cortical amyloid in cases of presenile and senile dementia
Cases of old-aged demented individuals exhibited abundant cortical amyloid deposits but only small numbers of neurofibrillary changes, which may represent a variant of Alzheimer's disease or an initial stage of this disorder.
The widespread alteration of neurites in Alzheimer's disease may be unrelated to amyloid deposition
It is demonstrated that a diffuse alteration of neurites similar to that present in AD takes place independently of the deposition of amyloid in SSPE, and this is consistent with the hypothesis that in AD, also, this alteration is not secondary to the depositing ofAmyloid.
Quantitative morphology and regional and laminar distributions of senile plaques in Alzheimer's disease
  • J. Rogers, J. Morrison
  • Biology
    The Journal of neuroscience : the official journal of the Society for Neuroscience
  • 1985
The finding that several different neurotransmitters can be immunocytochemically co-localized with plaques casts doubts on a primary role of cholinergic deterioration in plaque etiology, and opens the possibility that neocortical senile plaques may derive from pathologic events initiated in the neocortex.
Neurofibrillary degeneration and neuronal loss in alzheimer's disease
A variety of cerebral amyloid deposits in the brains of the Alzheimer-type dementia demonstrated byβ protein immunostaining
β protein immunostain with formic acid pretreatment is a useful method for the identification of a variety of senile cerebral amyloid deposits in patients with or without dementia and aged 17 to 91 years old.
Alzheimer's disease: Mismatch between amyloid plaques and neuritic plaques