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Association Between Visual Memory and In Vivo Amyloid and Tau Pathology in Preclinical Autosomal Dominant Alzheimer’s Disease

Published online by Cambridge University Press:  07 August 2020

Yamile Bocanegra
Affiliation:
Grupo de Neurociencias de Antioquia, Universidad de Antioquia, Calle 62 No. 52-59, Medellín, Colombia
Joshua T. Fox-Fuller
Affiliation:
Department of Psychiatry, Massachusetts General Hospital, Harvard Medical School, 100 1st Ave, Building 39, Suite 101, Charlestown, MA02129, USA Department of Psychological and Brain Sciences, Boston University, 900 Commonwealth Ave., 2nd Floor, Boston, MA02125, USA
Ana Baena
Affiliation:
Grupo de Neurociencias de Antioquia, Universidad de Antioquia, Calle 62 No. 52-59, Medellín, Colombia
Edmarie Guzmán-Vélez
Affiliation:
Department of Psychiatry, Massachusetts General Hospital, Harvard Medical School, 100 1st Ave, Building 39, Suite 101, Charlestown, MA02129, USA
Clara Vila-Castelar
Affiliation:
Department of Psychiatry, Massachusetts General Hospital, Harvard Medical School, 100 1st Ave, Building 39, Suite 101, Charlestown, MA02129, USA
Jairo Martínez
Affiliation:
Department of Psychiatry, Massachusetts General Hospital, Harvard Medical School, 100 1st Ave, Building 39, Suite 101, Charlestown, MA02129, USA
Heirangi Torrico-Teave
Affiliation:
Department of Psychiatry, Massachusetts General Hospital, Harvard Medical School, 100 1st Ave, Building 39, Suite 101, Charlestown, MA02129, USA
Francisco Lopera
Affiliation:
Grupo de Neurociencias de Antioquia, Universidad de Antioquia, Calle 62 No. 52-59, Medellín, Colombia
Yakeel T. Quiroz*
Affiliation:
Grupo de Neurociencias de Antioquia, Universidad de Antioquia, Calle 62 No. 52-59, Medellín, Colombia Department of Psychiatry, Massachusetts General Hospital, Harvard Medical School, 100 1st Ave, Building 39, Suite 101, Charlestown, MA02129, USA
*
*Correspondence and reprint requests to: Yakeel T. Quiroz, PhD, Associate Professor, Harvard Medical School, Departments of Psychiatry and Neurology, Massachusetts General Hospital, 100 1st Ave, Building 39, Suite 101, Charlestown, MA02129, USA. Phone: +(617) 643-5944, Fax: +(617) 726-5760. E-mail: yquiroz@mgh.harvard.edu

Abstract

Objective:

Visual memory (ViM) declines early in Alzheimer’s disease (AD). However, it is unclear whether ViM impairment is evident in the preclinical stage and relates to markers of AD pathology. We examined the relationship between ViM performance and in vivo markers of brain pathology in individuals with autosomal dominant AD (ADAD).

Methods:

Forty-five cognitively unimpaired individuals from a Colombian kindred with the Presenilin 1 (PSEN1) E280A ADAD mutation (19 carriers and 26 noncarriers) completed the Rey–Osterrieth Complex Figure immediate recall test, a measure of ViM. Cortical amyloid burden and regional tau deposition in the entorhinal cortex (EC) and inferior temporal cortex (IT) were measured using 11C-Pittsburgh compound B positron emission tomography (PET) and 11F-flortaucipir PET, respectively.

Results:

Cognitively unimpaired carriers and noncarriers did not differ on ViM performance. Compared to noncarriers, carriers had higher levels of cortical amyloid and regional tau in both the EC and IT. In cognitively unimpaired carriers, greater cortical amyloid burden, higher levels of regional tau, and greater age were associated with worse ViM performance. Only a moderate correlation between regional tau and ViM performance remained after adjusting for verbal memory scores. None of these correlations were observed in noncarriers.

Conclusions:

Results suggest that AD pathology and greater age are associated with worse ViM performance in ADAD before the onset of clinical symptoms. Further investigation with larger samples and longitudinal follow-up is needed to examine the utility of ViM measures for identifying individuals at high risk of developing dementia later in life.

Type
Regular Research
Copyright
Copyright © INS. Published by Cambridge University Press, 2020

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