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Clinical Manifestations.

Deepti Putcha1, Kanella Basilion2, Yuta Katsumi1

  • 1Frontotemporal Disorders Unit, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 24, 2025
PubMed
Summary
This summary is machine-generated.

Atypical Alzheimer's disease (AD) variants show memory encoding and storage deficits. Early-onset AD (EOAD) has faster memory loss, while posterior cortical atrophy (PCA) and logopenic variant primary progressive aphasia (lvPPA) differ in spatial memory binding.

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Area of Science:

  • Neuroscience
  • Neurology
  • Cognitive Science

Background:

  • Alzheimer's disease (AD) diagnostic criteria suggest preserved episodic memory in early stages, but memory deficits occur in atypical variants like posterior cortical atrophy (PCA) and logopenic variant primary progressive aphasia (lvPPA).
  • The distinct memory impairment patterns across non-amnestic AD syndromes remain unclear.
  • This study investigates memory deficits in early-onset AD (EOAD), lvPPA, and PCA.

Purpose of the Study:

  • To characterize and compare memory deficits in atypical Alzheimer's disease (AD) syndromes.
  • To investigate the shared and dissociable patterns of memory impairment.
  • To explore the relationship between brain atrophy and memory performance.

Main Methods:

  • 16 early-onset AD (EOAD), 9 lvPPA, 21 PCA, and 29 cognitively normal (CN) participants were tested.
  • A novel object-location memory test (OLMT) assessed associative memory without lexical demands.
  • Analysis of variance (ANOVA) and general linear models were used to analyze group performance and brain atrophy correlations.

Main Results:

  • All atypical AD variants showed impaired encoding and storage compared to controls.
  • EOAD exhibited greater storage loss at 3-minute recall than PCA and lvPPA.
  • lvPPA excelled at object-location association and retention, unlike EOAD and PCA, which struggled with encoding and retention of spatial locations.

Conclusions:

  • Atypical AD syndromes present with encoding and storage deficits, expanding the characterization of non-amnestic AD.
  • EOAD shows accelerated storage loss, suggesting potential multidomain impairment.
  • Distinct spatial memory binding deficits differentiate PCA and lvPPA, aiding in diagnosis and targeted cognitive training.