Area of research
Endocrine and Autonomic Systems · Biological Psychiatry
Research interest
Research topics from publications: Prophylactic melatonin significantly reduces Alzheimer’s neuropathology and associated cognitive deficits independent of antioxidant pathways in AβPPswe/PS1 mice; Genetic deletion of MT1/MT2 melatonin receptors enhances murine cognitive and motor performance; P3‐329: Effects of melatonin on cytoskeletal and synaptic proteins in an Alzheimer's mouse model. Representative work: BACKGROUND: Alzheimer's disease (AD) underlies dementia for millions of people worldwide, and its occurrence is set to double in the next 20 years. Currently, approved drugs for treating AD only marginally ameliorate cognitive deficits, and provide limited symptomatic relief, while newer substances under therapeutic development are potentially years away from benefiting patients. Melatonin (MEL) for insomnia has been proven safe with >15 years of over-the-counter access in the US. MEL exerts multiple complementary mechanisms of action against AD in animal models; thus it may be an excellent disease-modifying therapeutic. While presumed to provide neuroprotection via activation of known G-pro The pathogenesis of Alzheimer's disease (AD) remains controversial but it clearly involves the loss of neuronal homeostasis and synaptic activity with subsequent deficits in cognitive functions. Previous groups have reported that AD patients have decreased blood and CSF levels of melatonin. Lower CSF levels of melatonin have been strongly correlated with progression of AD neuropathology, and preclinical AD subjects already have decreased CSF melatonin levels. Several epidemiologic and case studies have also suggested that melatonin treatment provides cognitive benefit to MCI and AD patients. In our recent studies (Olcese et al., 2009; Dragicevic et al. 2011), we evaluated the neuroprotective