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P2‐341: THE COMBINED EFFECT OF COGNITIVE IMPAIRMENT AND PHYSICAL FRAILTY ON DEMENTIA INCIDENCE: SYSTEMATIC REVIEW AND META‐ANALYSIS
Author(s) -
Grande Giulia,
Haaksma Miriam L.,
Rizzuto Debora,
Melis René J.F.,
Marengoni Alessandra,
Onder Graziano,
Welmer Anna-Karin,
Pantoni Leonardo,
Fratiglioni Laura,
Vetrano Davide Liborio
Publication year - 2018
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2018.06.1031
Subject(s) - dementia , meta analysis , medicine , publication bias , confidence interval , gerontology , incidence (geometry) , population , cohort study , relative risk , cognitive decline , systematic review , medline , environmental health , disease , physics , political science , law , optics
were stratified into amyloid positive and amyloid negative groups using CSF biomarkers, with the cut off of 192pg/ml. FDG PET, MRI and neuropsychological assessment were conducted at baseline and at the 2-year follow-up. Cognitive decline was measured with a 3-point or more change on the ADAS-Cog and subsyndromal depressive symptoms were indexed with the self-rated geriatric depression scale. Path analysis was used to determine the relationships between depression, FDG and cognitive decline. Results: An increase in depressive symptoms was associated with faster cognitive decline and greater FDG hypometabolism in patients with MCI, with larger effects observed in patients with amyloid (cognitive decline OR1⁄4 5.99, p 1⁄4 .00; hypometabolism OR1⁄43.9,p1⁄4 .04), compared to patients without amyloid (cognitive decline OR1⁄4 3.1, p1⁄4 .03; hypometabolism OR1⁄4.08, p 1⁄4 .04). A mediation analysis indicated that in MCI patients with amyloid, an increase in depressive symptoms contributed to cognitive decline by contributing to FDG hypometabolism. In MCI patients without amyloid, hypometabolism did not mediate the relationship between depressive symptoms and cognitive decline. Conclusions: In MCI patients with amyloid pathology, depressive symptoms contributed to cognitive decline by reducing cerebral metabolism. Alternatively, in MCI patients without amyloid pathology, mechanisms other than neural degeneration may drive the effect of subsyndromal depression on cognitive decline, such as lack of motivation. Our findings support the idea that amyloid-associated depressive symptoms may be a prodromal stage of AD which may require different treatment strategies to non-amyloid associated depression.