Initial agonist treatment of Parkinson disease: a critique.

The evidence supporting initial dopamine agonist treatment of PD is reviewed. The two rationales for initial agonist treatment are reduced frequency of motor complications and possible relative neuroprotection by dopamine agonists. The basic science supporting these rationales is equivocal.

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.

Molecular and pathological effects of a modifier gene on deficiency of the sodium channel Scn8a (Na(v)1.6).

Scn8a encodes an abundant, widely distributed voltage-gated sodium channel found throughout the central and peripheral nervous systems. Mice with different mutant alleles of Scn8a provide models of the movement disorders ataxia, dystonia, tremor and progressive paralysis. We previously reported that the phenotype of the hypomorphic allele of Scn8a, medJ, is dependent upon an unlinked modifier locus, Scnm1.

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.

A mutation in the human neurofilament M gene in Parkinson's disease that suggests a role for the cytoskeleton in neuronal degeneration.

Parkinson's disease (PD) is a common neurodegenerative movement disorder characterized by the destruction of dopaminergic neurons of the substantia nigra. We have identified a new mutation (Gly336Ser) in the medium neurofilament subunit in a patient of French-Canadian origin with early onset severe PD. This finding suggests, for the first time, that aberrations in neuronal molecules involved in the cytoskeleton could lead to the development of the pathology seen in PD.

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.