Evidence map›Paper›PMID 40174910›Full record

ArticleNeuropathology and applied neurobiology2025

Pathological Characterisation of Posterior Cortical Atrophy in Comparison With Amnestic Alzheimer's Disease.

Z Abdi, K X Yong, J M Schott, A Gatt, T Revesz, S J Crutch, T Lashley

Abstract readComparative Study
PubMed Full text at PMC Publisher
In one paragraph

Article in Neuropathology and applied neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

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0cells of the map it votes in
4citing papers in PubMed
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1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Z AbdiDepartment of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, University College London, London, UK.ORCID 0000-0002-8979-5262
K X YongDementia Research Centre, Department of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, University College London, London, UK.
J M SchottDementia Research Centre, Department of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, University College London, London, UK.
A GattDepartment of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, University College London, London, UK.
T ReveszDepartment of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, University College London, London, UK.
S J CrutchDementia Research Centre, Department of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, University College London, London, UK.
T LashleyDepartment of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, University College London, London, UK.

Funding

Alzheimer's Society 382 (AS-CTF-17-001)
6 · The paper itself

Abstract

aimsPosterior cortical atrophy (PCA) is a predominantly young-onset neurodegenerative syndrome, typically caused by Alzheimer's disease (PCA-AD). PCA-AD presents with visual and spatial dysfunction attributed to occipito-parietal or 'posterior' brain regions rather than memory difficulties characteristic of typical amnestic-led Alzheimer's disease (a-AD) attributed to medial temporal regions. Imaging and neuropathological studies suggest that PCA-AD is associated with a more posterior distribution of tau neurofibrillary tangles (NFTs), whereas β-amyloid pathology (Aβ) is diffusely deposited throughout the cortex. This study characterised the neuropathological substrates of PCA-AD in comparison with a-AD, to further understanding of the biological basis of phenotypical heterogeneity in AD.

methodsImmunohistochemistry for Aβ; tau; the microglial markers CD68, CR3-43 and Iba1; α-synuclein; and TDP-43 was carried out on 26 PCA-AD and 27 age and gender-matched a-AD cases at the Queen Square Brain Bank. Aβ, tau and the three microglial markers were quantified in the superior frontal, superior temporal, superior parietal and occipital (primary visual cortex) cortices, with α-synuclein and TDP-43 assessed using formal staging criteria. In addition, microglial circularity, a morphological indicator of microglial activation state, was calculated.

resultsThere was a higher load of Aβ and tau in the parietal region of PCA-AD compared to a-AD. In the PCA-AD compared to the a-AD group, there were significant increases in tau load in parietal and frontal relative to temporal regions. There was no difference in cerebral amyloid angiopathy (CAA) severity between PCA-AD and a-AD. There was a significantly lower temporal CD68 load in a-AD compared with PCA-AD. In a-AD, CD68 load was lowest and tau load highest in the temporal relative to all other regions.

conclusionsThis study demonstrates differences in the distribution of Aβ and tau and variations in regional neuroinflammatory response in PCA-AD and a-AD. These findings extend our understanding of the biological substrates underpinning PCA-AD and highlight the potential for exploring phenotypic variants to understand selective vulnerability in neurodegenerative diseases.

Indexed as

Alzheimer DiseaseAmnesiaCerebral CortexAgedAged, 80 and overAmyloid beta-PeptidesAtrophyFemaleHumansMaleMicrogliaMiddle AgedNeurofibrillary Tanglestau ProteinsAmyloid beta-Peptidestau ProteinsAlzheimer's diseaseatypical Alzheimer's diseaseearly‐onset Alzheimer's diseaseposterior cortical atrophytypical Alzheimer's diseasevisual variant Alzheimer's disease

Identifiers

PMID40174910
PMCPMC11964714

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