Abstract
Alzheimer's disease (AD) is a progressive degenerative disease of the nervous system characterised neuropathologically by the presence of senile plaques and neurofibrillary tangles in amygdala, hippocampus and neocortex [1,2]. Dysfunction and death of basal cholinergic neurones projecting to forebrain targets are associated with marked decreases in cholinergic markers, including the activity of choline acetyl transferase [3]. Although cerebral cortical levels of somatostatin and somatostatin receptors have been reported to be reduced in AD, no consistent changes have been reported in other neuropeptide systems [4,5]. Here we review the current understanding of the role of corticotropin releasing factor (CRF) in AD and discuss the possibilities of exploiting this neuropeptide system for a molecular therapy to treat AD.