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Journal ArticleDOI

Neurofibrillary tangle-predominant dementia: comparison with classical Alzheimer disease

Kurt A. Jellinger, +1 more
- 23 Jan 2007 - 
- Vol. 113, Iss: 2, pp 107-117
TLDR
Neurofibrillary tangle predominant dementia (NFTPD) is a subset of late onset dementia, clinically different from traditional “plaque and tangle” Alzheimer disease (AD): later onset, shorter duration, less severe cognitive impairment, and almost absence of ApoE ε4.
Abstract
Neurofibrillary tangle predominant dementia (NFTPD) is a subset of late onset dementia, clinically different from traditional "plaque and tangle" Alzheimer disease (AD): later onset, shorter duration, less severe cognitive impairment, and almost absence of ApoE epsilon4. Neuropathology reveals abundant allocortical neurofibrillary pathology with no or few isocortical tau lesions, absence of neuritic plaques, absence or scarcity of amyloid deposits, but neurofibrillary changes comprising both 3 and 4 repeat (3R and 4R) tau immunohistochemistry are not significantly different from those in classical AD. Comparing 51 autopsy cases of NFTPD with 244 classical AD subjects, the nosology of NFTPD and its differences from AD are discussed.

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Citations
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Journal ArticleDOI

Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature

TL;DR: Evidence from many independent research centers strongly supports the existence of a specific disease, as defined by the presence of A&bgr; plaques and neurofibrillary tangles.
Journal ArticleDOI

Primary age-related tauopathy (PART): a common pathology associated with human aging

John F. Crary, +43 more
TL;DR: A new term is recommended, “primary age-related tauopathy” (PART), to describe a pathology that is commonly observed in the brains of aged individuals, yet this pathological process cannot be specifically identified pre-mortem at the present time.
Journal ArticleDOI

Classification and basic pathology of Alzheimer disease.

TL;DR: Tau accumulation, probably the best histopathological correlate of the clinical symptoms, takes three aspects: in the cell body of the neuron as neurofibrillary tangle, in the dendrites as neuropil threads, and in the axons forming the senile plaque neuritic corona.
Journal ArticleDOI

Neuropathologically defined subtypes of Alzheimer's disease with distinct clinical characteristics: a retrospective study.

TL;DR: H hippocampal sparing and limbic-predominant AD subtypes might account for about 25% of cases, and hence should be considered when designing clinical, genetic, biomarker, and treatment studies in patients with AD, and support the hypothesis that AD has distinct clinicopathological subtypes.
Journal ArticleDOI

The neuropathology of probable Alzheimer disease and mild cognitive impairment.

TL;DR: The objective of this study was to investigate single and mixed common age‐related neuropathologies in persons with probable AD and MCI.
References
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Journal ArticleDOI

Neuropathological stageing of Alzheimer-related changes.

Heiko Braak, +1 more
TL;DR: The investigation showed that recognition of the six stages required qualitative evaluation of only a few key preparations, permitting the differentiation of six stages.
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Gene dose of apolipoprotein E type 4 allele and the risk of Alzheimer's disease in late onset families

TL;DR: The APOE-epsilon 4 allele is associated with the common late onset familial and sporadic forms of Alzheimer9s disease (AD) in 42 families with late onset AD.
Journal ArticleDOI

Association of missense and 5′-splice-site mutations in tau with the inherited dementia FTDP-17

TL;DR: In this paper, the authors sequenced tau in FTDP-17 families and identified three missense mutations (G272V, P301L and R406W) and three mutations in the 5' splice site of exon in
Journal ArticleDOI

Staging of Alzheimer disease-associated neurofibrillary pathology using paraffin sections and immunocytochemistry.

TL;DR: To better meet the demands of routine laboratories this procedure is revised here by adapting tissue selection and processing to the needs of paraffin-embedded sections and by introducing a robust immunoreaction (AT8) for hyperphosphorylated tau protein that can be processed on an automated basis.
Journal ArticleDOI

Protective effect of apolipoprotein E type 2 allele for late onset Alzheimer disease.

TL;DR: A protective effect of the ε2 allele, in addition to the dose effect ofThe ε4 allele in sporadic AD, is demonstrated, which further support the direct involvement of APOE in the pathogenesis of AD.
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