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P4‐304: 18 F‐FDG‐PET HYPERACTIVITY IN ALZHEIMER'S DISEASE PRIMARY OLFACTORY CORTEX
Author(s) -
Meadowcroft Mark D.,
Purnell Carson J.,
Lu Jiaming,
Wang Jianli,
Karunanayaka Prasanna,
Yang Qing S.
Publication year - 2019
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.2019.06.5072
Subject(s) - anterior olfactory nucleus , piriform cortex , olfactory system , olfactory tubercle , neuroscience , amygdala , alzheimer's disease , positron emission tomography , temporal lobe , cerebellum , olfactory bulb , medicine , psychology , central nervous system , pathology , disease , epilepsy
F-fludeoxyglucose (FDG) positron emission tomography (PET) data from ADNI were analyzed to characterize metabolism in the olfactory region of AD (n1⁄416), mild-cognitive impaired (MCI) (N1⁄4149), and age-matched cognitively normal (CN) controls(N1⁄480). Results: In contrast to known medial and temporal lobe FDG hypo-metabolism within the AD default mode, a significant FDG hyper-metabolism was found in the primary olfactory cortex (POC) (including the piriform cortex, olfactory tubercle, anterior olfactory nucleus, and amygdala), nucleus accumbens, and cerebellum. The increase in POC glucose utilization was also shown in amyloid-positive MCI patients. The FDG-PET results are corroborated by an increase in fMRI signal fluctuation amplitude during resting state in these brain regions. Conclusions: The olfactory and cerebellar regions both contain inhibitory distal and inter-neuronal connections that are vulnerable to disruption in AD. The hyper-metabolism in the olfactory structures and cerebellum may reflect disruption of local and system-wide inhibitory networks due to AD neurodegeneration, suggesting a hypothetical mechanism for susceptibility of the olfactory system to early AD.