A major focus of Dr. Pomara’s research has been to elucidate pharmacokinetic and pharmacodynamic factors that may contribute to individual vulnerability to drug induced cognitive and psychomotor toxicity in the elderly. He has shown that certain variants of the APOE and TOMM40 genes increase risk for drug-induced adverse events unrelated to pharmacokinetic factors and likely reflecting pharmacodynamic mechanisms.
Other important contributions include his early reports of increased activity in the HPA axis associated with both aging and AD, as determined by studies of baseline cortisol and dexamethasone response. These results led to the first pilot clinical trial that examined the cognitive effects of the glucocorticoid receptor antagonist, RU486, in AD. Dr. Pomara also provided the first report on an absence of a cortisol response to naltrexone and an elevation in CSF-glutamate in Alzheimer’s patients.
Dr. Pomara additionally presented the first evidence that late life depression, a condition associated with increased risk for Alzheimer’s disease (AD) or prodromal phase, may be accompanied by disturbances in central and peripheral metabolism of amyloid-beta, a peptide implicated in AD. More recently, he has been collaborating with the NYU Cohen Veterans Center to identify biomarkers for PTSD/TBI.
Professor, Department of Psychiatry
Professor, Department of Pathology
Psychiatry research. 2017 Apr 23; 264:76-81
Selective and state-dependent changes in CSF abeta42 levels in cognitively-intact elderly with late life major depression [Meeting Abstract]
Neuropsychopharmacology. 2016 Dec; Conference:(55th):S544
Journal of clinical & experimental neuropsychology. 2016 Nov; 38(9):967-973
Neuropsychology. 2016 Nov; 30(8):906-914
Neuroreport. 2016 Sep 28; 27(14):1068-1071
American journal of geriatric psychiatry. 2016 Sep; 24(9):773-775
Neuroreport. 2016 Aug 03; 27(11):869-873
Translational psychiatry. 2016 Mar 01; 6:e744-e744e744