S. Lloyd

TL;DR: A genetic predisposition to lower D2 receptor expression may increase susceptibility to neuroleptic medication or clinical symptoms that are associated with diseases involving dopaminergic pathology.

TL;DR: Investigation of dopaminergic activities along the rostrocaudal striatal axis from a post-mortem series indicated compensatory increased turnover in Parkinson's disease, which was absent in DLB despite the loss of substantia nigra neurons, dopamine and uptake sites.

TL;DR: It is concluded that widespread abnormalities of thalamic nicotine are not implicated in schizophrenia or DLB, but that reticular αBGT binding may be involved to a lesser and greater extent in the pathophysiology or psychopathology of both disorders.

TL;DR: The changes observed in [3H]nicotine binding are likely to reflect the presence of these receptors on multiple sites within the striatum, which may be differentially modulated in the different diseases.

TL;DR: Findings implicate mechanisms controlling the expression of nicotinic receptors to a greater extent than muscarinic receptors in postnatal development and aging in the human hippocampus.