OBJECTIVE: An ascendant body of evidence suggests that Alzheimer disease with psychosis (AD+P) is a distinct variant of illness with its own genetic diathesis and a unique clinical course. Impaired frontal lobe function has been previously implicated in AD+P. The current exploratory study, presented in two parts, evaluates both the regional brain metabolic and psychometric correlates of psychosis in a longitudinal sample of subjects with AD, made available by the Alzheimer's Disease Neuroimaging Initiative (ADNI). METHODS: In Part 1 of the study, 21 ADNI participants with AD who developed psychotic symptoms during the study but were not psychotic at baseline were matched with 21 participants with AD who never became psychotic during the study period, and mean brain [F(18)]fluorodeoxyglucose positron emission tomography (FDG-PET) Cerebral metabolic rate for glucose (CMRgl) by regions of interest (ROIs) were compared Additionally, 39 participants with active psychosis at the time of image acquisition were matched with 39 participants who were never psychotic during the study period, and mean brain FDG-PET CMRgl by sROI were compared. In Part 2 of the study, 354 ADNI participants with AD who were followed for 24 months with serial psychometric testing were identified, and cognitive performance and decline were evaluated for correlation with psychotic symptoms. RESULTS: Part 1: There were no regional brain metabolic differences between those with AD destined to become psychotic and those who did not become psychotic. There was a significant reduction in mean orbitofrontal brain metabolism in those with active psychosis. Part 2: Over the course of study follow-up, psychosis was associated with accelerated decline in functional performance as measured by the Functional Assessment Questionnaire, the Mini-Mental State Examination, and Forward Digit Span. CONCLUSION: In a sample drawn from the ADNI dataset, our exploratory FDG-PET findings and longitudinal cognitive outcomes support the hypofrontality model of AD+P. Focal frontal vulnerability may mediate the accelerated decline seen in AD+P.
OBJECTIVE: An ascendant body of evidence suggests that Alzheimer disease with psychosis (AD+P) is a distinct variant of illness with its own genetic diathesis and a unique clinical course. Impaired frontal lobe function has been previously implicated in AD+P. The current exploratory study, presented in two parts, evaluates both the regional brain metabolic and psychometric correlates of psychosis in a longitudinal sample of subjects with AD, made available by the Alzheimer's Disease Neuroimaging Initiative (ADNI). METHODS: In Part 1 of the study, 21 ADNI participants with AD who developed psychotic symptoms during the study but were not psychotic at baseline were matched with 21 participants with AD who never became psychotic during the study period, and mean brain [F(18)]fluorodeoxyglucose positron emission tomography (FDG-PET) Cerebral metabolic rate for glucose (CMRgl) by regions of interest (ROIs) were compared Additionally, 39 participants with active psychosis at the time of image acquisition were matched with 39 participants who were never psychotic during the study period, and mean brain FDG-PET CMRgl by sROI were compared. In Part 2 of the study, 354 ADNI participants with AD who were followed for 24 months with serial psychometric testing were identified, and cognitive performance and decline were evaluated for correlation with psychotic symptoms. RESULTS: Part 1: There were no regional brain metabolic differences between those with AD destined to become psychotic and those who did not become psychotic. There was a significant reduction in mean orbitofrontal brain metabolism in those with active psychosis. Part 2: Over the course of study follow-up, psychosis was associated with accelerated decline in functional performance as measured by the Functional Assessment Questionnaire, the Mini-Mental State Examination, and Forward Digit Span. CONCLUSION: In a sample drawn from the ADNI dataset, our exploratory FDG-PET findings and longitudinal cognitive outcomes support the hypofrontality model of AD+P. Focal frontal vulnerability may mediate the accelerated decline seen in AD+P.
Authors: Winnie Qian; Tom A Schweizer; Nathan W Churchill; Colleen Millikin; Zahinoor Ismail; Eric E Smith; Lisa M Lix; David G Munoz; Joseph J Barfett; Tarek K Rajji; Corinne E Fischer Journal: Am J Geriatr Psychiatry Date: 2018-10-02 Impact factor: 4.105
Authors: Jeremy Koppel; Heidy Jimenez; Leslie Adrien; Eric H Chang; Anil K Malhotra; Peter Davies Journal: J Neurochem Date: 2018-11-12 Impact factor: 5.372
Authors: Michael W Weiner; Dallas P Veitch; Paul S Aisen; Laurel A Beckett; Nigel J Cairns; Robert C Green; Danielle Harvey; Clifford R Jack; William Jagust; John C Morris; Ronald C Petersen; Andrew J Saykin; Leslie M Shaw; Arthur W Toga; John Q Trojanowski Journal: Alzheimers Dement Date: 2017-03-22 Impact factor: 21.566
Authors: Ann Kolanowski; Marie Boltz; Elizabeth Galik; Laura N Gitlin; Helen C Kales; Barbara Resnick; Kimberly S Van Haitsma; Amy Knehans; Jane E Sutterlin; Justine S Sefcik; Wen Liu; Darina V Petrovsky; Lauren Massimo; Andrea Gilmore-Bykovskyi; Margaret MacAndrew; Glenna Brewster; Vycki Nalls; Ying-Ling Jao; Naomi Duffort; Danny Scerpella Journal: Nurs Outlook Date: 2017-06-16 Impact factor: 3.250
Authors: Michael W Weiner; Dallas P Veitch; Paul S Aisen; Laurel A Beckett; Nigel J Cairns; Jesse Cedarbaum; Robert C Green; Danielle Harvey; Clifford R Jack; William Jagust; Johan Luthman; John C Morris; Ronald C Petersen; Andrew J Saykin; Leslie Shaw; Li Shen; Adam Schwarz; Arthur W Toga; John Q Trojanowski Journal: Alzheimers Dement Date: 2015-06 Impact factor: 21.566
Authors: Jeremy Koppel; Chris Acker; Peter Davies; Oscar L Lopez; Heidy Jimenez; Miriam Azose; Blaine S Greenwald; Patrick S Murray; Caitlin M Kirkwood; Julia Kofler; Robert A Sweet Journal: Neurobiol Aging Date: 2014-03-06 Impact factor: 4.673