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Pathologic substrate, risk factors, and functional impact of delusions and hallucinations in neuropathologically diagnosed Alzheimer's disease

Published online by Cambridge University Press:  10 December 2015

D. G. Munoz ,
W. Qian ,
T. A. Schweizer  and
C.E. Fischer
D. G. Munoz
Affiliation:
Keenan Research Centre for Biomedical Research, Li Ka Shing Knowledge Institute, St. Michael's Hospital, Toronto, ON
W. Qian
Affiliation:
Keenan Research Centre for Biomedical Research, Li Ka Shing Knowledge Institute, St. Michael's Hospital, Toronto, ON
T. A. Schweizer
Affiliation:
Keenan Research Centre for Biomedical Research, Li Ka Shing Knowledge Institute, St. Michael's Hospital, Toronto, ON
C.E. Fischer
Affiliation:
Keenan Research Centre for Biomedical Research, Li Ka Shing Knowledge Institute, St. Michael's Hospital, Toronto, ON
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Abstract

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Information
Canadian Journal of Neurological Sciences , Volume 42 , Issue S3: ABSTRACTS: 55th Annual Canadian Association of Neuropathologists Meeting , December 2015 , pp. S3
Copyright
Copyright © The Canadian Journal of Neurological Sciences Inc. 2015 

Utilizing the National Alzheimer’s Coordinating Center database we analyzed 728 patients with Alzheimer's disease (AD), neuropathologically confirmed based on the CERAD criteria, comparing those (n=271) that at any moment in their evolution suffered delusions or hallucinations (P+) versus those (n=457) that did not (P-). There was no difference in AD lesion load. P+ subjects had a higher prevalence of subcortical arteriosclerotic leukoencephalopathy (SAL) and, as expected, higher Lewy body stage. Hypertension was more common in P+ patients and diabetes in subjects with both delusions and hallucinations. P+ patients tended to quit smoking later in life. The functional associations diverged: patients with delusions only had better CDR, MMSE and FAQ than P-patients, whereas the opposite was true for patients with hallucinations, whether isolated or associated with delusions. In contrast, an overlapping sample of 890 subjects from the same database with a clinical diagnosis of AD and available neuropathological exam showed greater AD load in the P+ group, a result we interpret as due to clinical misdiagnosis, since the P- group was enriched in subjects with a Braak stage I and II. We conclude that SAL is, along with Lewy bodies, a substrate for psychotic symptoms in AD, and that vascular risk factors are likely to contribute to the development of this condition.

Conflictsof Interest:

None.