3.9 Article

Behavioural disorders in Alzheimer's disease: the descriptive and predictive role of brain 18F-fluorodesoxyglucose-positron emission tomography

Journal

PSYCHOGERIATRICS
Volume 21, Issue 4, Pages 514-520

Publisher

WILEY
DOI: 10.1111/psyg.12699

Keywords

Alzheimer' s disease; BPSD; brain FDG‐ PET; dementia

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Alzheimer's disease (AD) has a high incidence in the elderly population, with behavioural and psychological symptoms of dementia (BPSD) being common. This study found that positive BPSD, including aggression/agitation and psychotic symptoms, were frequently observed in AD patients, with the temporal lobes identified as a key region involved in these symptoms and FDG-PET showing potential in predicting their development.
Background Alzheimer's disease (AD) has a high incidence in the elderly. Besides cognitive disorders, patients may also develop behavioural and psychological symptoms of dementia (BPSD), which can be particularly disabling for patients and families. BPSD encompass a wide range of symptoms, among which psychotic symptoms and disruptive behaviours often prompt the first related hospitalization and request for family support. The aetiological mechanism of BPSD has not yet been clarified, and no predictive or risk factors have been identified. The main objectives of our study are to describe the frequency of aggression/agitation and psychotic symptoms, defined 'positive BPSD', in a cohort of 60 AD patients, identify areas of the brain involved in behavioural symptomatology through brain F-18-fluorodesoxyglucose-positron emission tomography (FDG-PET), and investigate a potential predictive role of brain FDG-PET in BPSD development. Methods A cohort of 60 AD patients was retrospectively enrolled and regularly followed for at least 3 years. Each subject underwent brain FDG-PET at the time of diagnosis. Patients were divided into three groups based on the presence of behavioural disturbances: present, absent, and developed later. Results Of the 60 AD patients in the cohort, 52% had positive BPSD: 17 at baseline and 14 during the 3-year follow-up. FDG-PET identified an association between hypometabolism in the bilateral temporal lobes and the presence of BPSD, and showed initial hypometabolism in the postero-temporal lobes 3 years before symptom onset. Conclusions Positive BPSD are frequently manifested in AD. Our study identified the temporal lobes as the neurobiological substrate of positive BPSD and FDG-PET as a potential instument to predict their developement. Temporal lobes are involved in processing facial expression and recognizing emotions; an impairment of these functions could cause delusions and agitated/aggressive behaviour. To confirm the potential predictive role of FDG-PET in the onset of BPSD in AD, further studies are needed.

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