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Posterior cortical atrophy (PCA) is a neurodegenerative disorder primarily associated with Alzheimer’s disease (AD) pathology. In contrast with the predominantly amnestic profile of typical AD, the central feature of PCA is an impairment of visuospatial cognition. In addition to this core deficit, there is growing consensus that other cognitive domains such as language and memory can also be impaired in the early stages of the disease,1 2 providing supplementary markers to diagnosis. The evolution of these cognitive symptoms over time, however, has received limited investigation. An understanding of the profile and measurement of progression of cognitive symptoms in PCA is crucial for clinicians to determine the level and type of support needed at different stages of the disease. In addition, the identification of reliable measures of disease progression is vital for determining the efficacy of treatments in clinical trials. The current study aimed to (1) characterise the pattern of cognitive decline over time in PCA, and (2) evaluate the potential of a well-validated screening tool for monitoring short-term and long-term cognitive changes in clinical and research settings.
Methods and materials
Eighteen patients (eight women) with PCA were recruited from the Oxford Cognitive Disorders Clinic, UK, and the Research Institute for the Care of Older People, Bath, UK. Seventeen healthy demographically-matched controls (eight women) were recruited from the community. All participants completed the Addenbrooke’s Cognitive Examination-Revised (ACE-R)3 and/or Addenbrooke’s Cognitive Examination-III (ACE-III)4 on two or more time points (M=4.2, SD ±1.3), with assessments being conducted 3 months apart or more (M=21.5, SD ±9.7). Cognitive subdomains assessed by the ACE are orientation/attention, memory, …
Twitter @MargotOverman, @NikJDrummond
Contributors MJO analysed the data and wrote the manuscript. ND contributed to data collection and revision of the manuscript. CRB contributed to revision of the manuscript. SA designed the study, contributed to data acquisition and revised the manuscript.
Funding SA was supported by Alzheimer’s Research UK (ARUK-NSG2017-4). CRB was supported by a Medical Research Council Clinician Scientist Fellowship (MR/K010395/1).
Competing interests None declared.
Provenance and peer review Not commissioned; externally peer reviewed.
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