pharmacogenetics, Alzheimer's disease, drug-induced cognitive toxicity, late-life depression
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.
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Translational psychiatry. 2022 Jul 28; 12(1):301
Neuropsychology. 2022 Jan 01; ?-?
Journal of Alzheimer's disease. 2022 01 ; 85(3):1267-1282