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Neurobiol Aging. 2019 Aug 14;84:61-69. doi: 10.1016/j.neurobiolaging.2019.08.008. [Epub ahead of print]

Benzodiazepine use and brain amyloid load in nondemented older individuals: a florbetapir PET study in the Multidomain Alzheimer Preventive Trial cohort.

Author information

1
UMR 1253, iBrain, Université de Tours, Inserm, Tours, France; CHU de Tours, Tours, France. Electronic address: t.desmidt@chu-tours.fr.
2
Department of Geriatrics, Gérontopôle, CHU Toulouse, Purpan University Hospital, Toulouse, France; UMR1027, Université de Toulouse, UPS, INSERM, Toulouse, France.
3
University of Lille, Inserm U1171, CHU, DistalZ, Lille, France.
4
Behavior and Basal Ganglia host team 4712, University of Rennes 1, Rennes, France; Department of Psychiatry, Rennes University Hospital, Guillaume Régnier Hospital Centre, Rennes, France.
5
Department of Psychiatry, Memory Research and Resources Center, CHU Nice, Nice, France.
6
CHU de Tours, Tours, France.
7
UMR 1253, iBrain, Université de Tours, Inserm, Tours, France.
8
UMR 1253, iBrain, Université de Tours, Inserm, Tours, France; INSERM CIC 1415, Université de Tours, Tours, France; CHRU de Tours, Unité de Radiopharmacie, Tours, France.
9
UMR 1253, iBrain, Université de Tours, Inserm, Tours, France; CHU de Tours, Tours, France; INSERM CIC 1415, Université de Tours, Tours, France.
10
UMR 1214, Toulouse Neuroimaging Center, University of Toulouse III, Toulouse, France; Department of Nuclear Medicine, University Hospital of Toulouse (CHU Toulouse), Toulouse, France.
11
CHU de Tours, Tours, France; INSERM CIC 1415, Université de Tours, Tours, France.
12
UMR 1253, iBrain, Université de Tours, Inserm, Tours, France; CHU de Tours, Tours, France.

Abstract

It remains unclear whether benzodiazepines (BZDs) constitute a risk factor for Alzheimer's disease (AD). In this study, we investigated associations between chronic use of BZDs and brain amyloid load, a hallmark of AD, in 268 nondemented older individuals. F18-florbetapir positron emission tomography scans were performed to assess amyloid load as measured by standardized uptake value ratios, which were compared between chronic BZD users and nonusers using adjusted multiple linear regressions. Short- versus long-acting BZDs were also considered in the analyses. Standardized uptake value ratios were significantly lower in BZD users (n = 47) than in nonusers (n = 221), independent of multiple adjustments. The effect was stronger for short-acting BZDs than for long-acting BZDs. This is the first large clinical study showing a reduced brain amyloid load in chronic BZD users, especially with short-acting BZDs. Our results do not support the view of BZD use as a risk factor for AD and instead support the involvement of pharmacological mechanisms related to neuronal hyperactivity, neuroinflammation, and sleep quality as potential targets for blocking amyloid accumulation.

KEYWORDS:

Alzheimer's disease; Amyloid; Benzodiazepine; Florbetapir; GABA-A; Positron emission tomography

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