Temporoparietal atrophy: A marker of AD pathology independent of clinical diagnosis

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Abstract

Alzheimer's disease (AD) can present with non-amnestic clinical syndromes. We investigated whether there is an imaging signature of AD pathology in these atypical subjects. We identified 14 subjects that had pathological AD, a non-amnestic presentation (i.e. atypical AD), and MRI. These subjects were matched to 14 with clinical and pathological AD (i.e. typical AD), 14 with the same non-amnestic presentations with frontotemporal lobar degeneration (FTLD) pathology, and 20 controls. Voxel-based morphometry and region-of-interest (ROI) analysis were used to assess patterns of grey matter loss. Loss was observed in the temporoparietal cortex in both typical and atypical AD, and showed significantly greater loss than FTLD. However, the medial temporal lobes were more severely affected in typical AD and FTLD compared to atypical AD. A ratio of hippocampal and temporoparietal volumes provided excellent discrimination of atypical AD from FTLD subjects. Temporoparietal atrophy may therefore provide a useful marker of the presence of AD pathology even in subjects with atypical clinical presentations, especially in the context of relative sparing of the hippocampus.

Original languageEnglish (US)
Pages (from-to)1531-1541
Number of pages11
JournalNeurobiology of Aging
Volume32
Issue number9
DOIs
StatePublished - Sep 2011

Fingerprint

Clinical Pathology
Atrophy
Alzheimer Disease
Frontotemporal Lobar Degeneration
Pathology
Temporal Lobe
Hippocampus

Keywords

  • Alzheimer's disease
  • Frontotemporal lobar degeneration
  • Hippocampus
  • Non-amnestic presentation
  • Pathology
  • Temporoparietal cortex
  • Voxel-based morphometry

ASJC Scopus subject areas

  • Clinical Neurology
  • Neuroscience(all)
  • Aging
  • Developmental Biology
  • Geriatrics and Gerontology

Cite this

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title = "Temporoparietal atrophy: A marker of AD pathology independent of clinical diagnosis",
abstract = "Alzheimer's disease (AD) can present with non-amnestic clinical syndromes. We investigated whether there is an imaging signature of AD pathology in these atypical subjects. We identified 14 subjects that had pathological AD, a non-amnestic presentation (i.e. atypical AD), and MRI. These subjects were matched to 14 with clinical and pathological AD (i.e. typical AD), 14 with the same non-amnestic presentations with frontotemporal lobar degeneration (FTLD) pathology, and 20 controls. Voxel-based morphometry and region-of-interest (ROI) analysis were used to assess patterns of grey matter loss. Loss was observed in the temporoparietal cortex in both typical and atypical AD, and showed significantly greater loss than FTLD. However, the medial temporal lobes were more severely affected in typical AD and FTLD compared to atypical AD. A ratio of hippocampal and temporoparietal volumes provided excellent discrimination of atypical AD from FTLD subjects. Temporoparietal atrophy may therefore provide a useful marker of the presence of AD pathology even in subjects with atypical clinical presentations, especially in the context of relative sparing of the hippocampus.",
keywords = "Alzheimer's disease, Frontotemporal lobar degeneration, Hippocampus, Non-amnestic presentation, Pathology, Temporoparietal cortex, Voxel-based morphometry",
author = "Whitwell, {Jennifer Lynn} and Jack, {Clifford R Jr.} and Przybelski, {Scott A.} and Parisi, {Joseph E} and Senjem, {Matthew L.} and Boeve, {Bradley F} and Knopman, {David S} and Petersen, {Ronald Carl} and Dickson, {Dennis W} and Josephs, {Keith Anthony}",
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T2 - A marker of AD pathology independent of clinical diagnosis

AU - Whitwell, Jennifer Lynn

AU - Jack, Clifford R Jr.

AU - Przybelski, Scott A.

AU - Parisi, Joseph E

AU - Senjem, Matthew L.

AU - Boeve, Bradley F

AU - Knopman, David S

AU - Petersen, Ronald Carl

AU - Dickson, Dennis W

AU - Josephs, Keith Anthony

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AB - Alzheimer's disease (AD) can present with non-amnestic clinical syndromes. We investigated whether there is an imaging signature of AD pathology in these atypical subjects. We identified 14 subjects that had pathological AD, a non-amnestic presentation (i.e. atypical AD), and MRI. These subjects were matched to 14 with clinical and pathological AD (i.e. typical AD), 14 with the same non-amnestic presentations with frontotemporal lobar degeneration (FTLD) pathology, and 20 controls. Voxel-based morphometry and region-of-interest (ROI) analysis were used to assess patterns of grey matter loss. Loss was observed in the temporoparietal cortex in both typical and atypical AD, and showed significantly greater loss than FTLD. However, the medial temporal lobes were more severely affected in typical AD and FTLD compared to atypical AD. A ratio of hippocampal and temporoparietal volumes provided excellent discrimination of atypical AD from FTLD subjects. Temporoparietal atrophy may therefore provide a useful marker of the presence of AD pathology even in subjects with atypical clinical presentations, especially in the context of relative sparing of the hippocampus.

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