Cerebral Amyloid Deposition and Serotoninergic Innervation in Parkinson Disease

Abstract

Production and deposition of β-amyloid (Aβ) are probably central to the pathogenesis of Alzheimer disease and related disorders such as dementia with Lewy bodies. Experimental evidence suggests that Aβ production is modulated by synaptic activity and by activation of specific neurotransmitter receptors, including N -methyl-D–aspartic acid receptors, M1 muscarinic cholinergic receptors, and serotonin receptors.1-5 Recent animal studies suggest that augmentation of serotoninergic neurotransmission by selective serotonin reuptake inhibitors (SSRIs) may have a neuroprotective influence on the development of cerebral amyloidopathy.6 Cirrito et al6 also reported retrospective human data suggesting that SSRI use reduced Aβ deposition in humans as measured by carbon 11 ([11C])–labeled Pittsburgh compound B (PiB) positron emission tomography (PET).