Procedure guideline for brain death scintigraphy.
Explore the source record for details and available documents.
Brain↗
Biomedical subjects
Kirk A Frey
Publications and source records attributed to Kirk A Frey.
Brain imaging to assess the effects of dopamine agonists on progression of Parkinson disease.
Explore the source record for details and available documents.
Antiparkinson Agents↗
Cholinergic vesicular transporters in progressive supranuclear palsy.
OBJECTIVE: To determine the status of cholinergic and monoaminergic vesicular transporter binding sites in progressive supranuclear palsy (PSP). METHODS: The authors determined autoradiographically the regional expression of acetylcholine vesicular transporter (VAChT) and monoamine vesicular transporter type 2 (VMAT2) binding sites in postmortem basal ganglia samples from subjects with PSP. Comparison neurochemical measures included choline acetyltransferase (ChAT) enzyme activity and benzodiazepine (BZ) binding sites. RESULTS: VAChT expressions and ChAT activities in caudate nucleus and putamen were markedly decreased in PSP, whereas BZ binding was unaffected, consistent with selective losses of striatal cholinergic interneurons. VMAT2 density was reduced significantly in the caudate nucleus, putamen, and substantia nigra pars compacta, consistent with degeneration of dopaminergic nigrostriatal projection neurons in PSP. In the globus pallidus, BZ receptor binding sites were reduced, whereas VMAT2 and VAChT binding sites were unchanged, indicating losses of intrinsic pallidal neurons and synapses. CONCLUSIONS: These results confirm selective and marked degenerations of basal ganglia cholinergic and dopaminergic terminals in PSP. Striatal VAChT reduction may provide a unique neurochemical imaging marker for distinction of PSP from other types of basal ganglia neurodegeneration.
Acetylcholine↗
Can SPET imaging of dopamine uptake sites replace PET imaging in Parkinson's disease? Against.
Explore the source record for details and available documents.
Biomarkers↗
Striatal monoaminergic terminals in Lewy body and Alzheimer's dementias.
Vesicular monoamine transporter type 2 and benzodiazepine binding site expressions were examined with quantitative autoradiography in postmortem striata from 19 patients with dementia with Lewy bodies, seven patients with dementia with Lewy bodies and Alzheimer's disease, 12 patients with Alzheimer's disease, and eight neurologically normal subjects. Striatal vesicular monoamine transporter type 2 expression in dementia with Lewy bodies and in dementia with Lewy bodies plus Alzheimer's disease was reduced significantly, indicating degeneration of nigrostriatal projections. Striatal benzodiazepine binding site expression was unchanged, indicating preserved intrinsic striatal neuropil. Vesicular monoamine transporter type 2 and benzodiazepine binding site expressions were each preserved in Alzheimer's disease striatum. We conclude that dementia with Lewy bodies may be distinguished from Alzheimer's disease by postmortem examination or by future in vivo measurements of the striatal vesicular monoamine transporter type 2.
Aged↗
Stable beta-secretase activity and presynaptic cholinergic markers during progressive central nervous system amyloidogenesis in Tg2576 mice.
We examined presynaptic cholinergic markers and beta-secretase activity during progressive central nervous system amyloidogenesis in Tg2576 Alzheimer mice (transgenic for human amyloid precursor protein Swedish mutation; hAPPswe). At 14, 18, and 23 months of age there were no significant differences between wild-type and transgenic mice in four distinct central nervous system cholinergic indices--choline acetyltransferase and acetylcholinesterase activities, and binding to vesicular acetylcholine transporter and Na(+)-dependent high-affinity choline uptake sites. A novel enzyme-linked immunosorbent assay measuring only the secreted human beta-secretase cleavage product (APPsbetaswe) of APPswe also revealed no change with aging in Tg2576 mouse brain. In contrast, transgenic but not wild-type mice exhibited an age-dependent increase in soluble Abeta40 and Abeta42 levels and progressive amyloid deposition in brain. Thus, aging Tg2576 mice exhibited presynaptic cholinergic integrity despite progressively increased soluble Abeta40 and Abeta42 levels and amyloid plaque density in brain. Older Tg2576 mice may best resemble preclinical or early stages of human Alzheimer's disease with preserved presynaptic cholinergic innervation. Homeostatic APPsbetaswe levels with aging suggest that progressive amyloid deposition in brain results not from increased beta-secretase cleavage of APP but from impaired Abeta/amyloid clearance mechanisms.
Acetylcholinesterase↗
Neuroimaging in dementia with Lewy bodies: metabolism, neurochemistry, and morphology.
Dementia with Lewy bodies (DLB) is recognized as one of the most common forms of neurodegenerative dementia. Neuroimaging contributes to a better understanding of the pathophysiology of DLB by examining alterations in brain metabolism, neurochemisty, and morphology in living patients. Neuroimaging can provide objective and quantifiable antemortem markers for the presence of and the progression of DLB and permits differentiation from other dementias. This article reviews current neuroimaging findings in DLB with particular attention to occipital hypometabolism, dopaminergic and cholinergic deficits, and medial temporal lobe atrophy as measured by positron emission tomography, single-photon emission computed tomography, and magnetic resonance imaging.
Aged↗