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Imaging of synaptic functions in Parkinson Plus syndromes
This is my new favorite abstract as it addresses diagnosing people on the basis of synaptic neurotransmission. Perhaps there is a unique synaptic profile for each disorder. The abstract also addresses in part the issue of whether there's dysfunction in the sending of a signal in the brain or the receiving of a signal in the brain. This research is out of Germany.
Behavioral Brain Research. 2009 Jun 9. [Epub ahead of print]
In vivo imaging of synaptic function in the central nervous system. I. Movement disorders and dementia.
Nikolaus S, Antke C, MÃ¼ller HW.
Clinic of Nuclear Medicine, University Hospital DÃ¼sseldorf, Heinrich-Heine University, DÃ¼sseldorf, Germany.
This review gives an overview of those in vivo imaging studies on synaptic neurotransmission, which so far have been performed on patients with movement disorders and/or dementia. Thereby, the focus is on disease-related deficiencies within the functional entity of the dopaminergic, serotonergic, cholinergic, glutamatergic, GABAergic or opioid synapse. In vivo investigations have yielded highly consistent results on the dysfunction of synaptic constituents in the majority of diseases covered by this overview.
Findings show presynaptic dysfunctions in idiopathic as well as early-onset Parkinson's disease with decreases in striatal dopamine synthesis (57 out of a total of of 59 reports on both types of Parkinson's disease), storage (9 out of 9 reports), release (2 out of 3 reports) and transporter binding (95 out of 95 reports).
In contrast, the "Parkinson plus" syndromes multiple system atrophy and progressive supranuclear palsy are characterized by both pre- and postsynaptic deficiencies with reductions in striatal dopamine synthesis (11 out of a total of 11 reports on both types of "Parkinson plus" syndromes), storage (4 of 4 reports), and transporter binding (27 out of 27 reports) as well as D(1) (2 out of 2 reports) and D(2) receptor binding (34 out of 36 reports).
This does not hold for the "Parkinson plus" syndromes dementia with Lewy bodies and corticobasal degeneration. For these diseases, for the time being, firm evidence of alterations in D(1) and/or D(2) receptor binding is lacking.
In patients with Huntington's disease, mainly postsynaptic dysfunctions with reductions of striatal D(1) (6 out of 6 reports) and D(2) receptor binding (15 out of 15 reports) were observed.
Alzheimer's disease is characterized by both pre-and postsynatic deficiences of the cholinergic system with decreases of cortical acetylcholine storage (1 out of 2 reports) and both musarinic (7 out of 10 reports) and nicotinic cholinergic receptor binding (3 out of 6 reports). Moreover, reductions in cortical (1 out of 3 reports) and limbic 5-HT(1A) (3 out of 3 reports) and cortical (4 out of 4 reports) and limbic 5-HT(2A) receptor binding (1 out of 2 reports) were observed. Moreover, there is evidence for a cortical (4 out of 6 reports) and cingulate (3 out of 3 reports) increase of peripheral benzodiazepine receptor binding indicative of microglial activation.
In the majority of investigations on patients with Alzheimer's disease, no alterations of presynaptic dopamine function were found, whereas all other forms of dementia including corticobasal degeneration, dementia with Lewy bodies, Parkinson's disease dementia and frontotemporal dementia were characterized by presynatic dopaminergic deficiencies with reductions in striatal dopamine synthesis (10 out of a total of 10 reports on these types of dementia), storage (4 out of 4 reports) and transporter binding (29 out of 29 reports).
Taken together, in vivo imaging methods can be employed for the diagnosis of idiopathic and early-onset Parkinson's disease as well as "Parkinson plus" syndromes and Huntington's disease. Moreover, differentiation is feasible between, firstly, Parkinson's disease and the "Parkinson plus" syndromes multiple system atrophy and progressive supranuclear palsy, secondly, multiple system atrophy/progressive supranuclear palsy and the other "Parkinson plus" syndromes dementia with Lewy bodies and corticobasal degeneration, and, thirdly, Alzheimer's disease and other forms of dementia.
PubMed ID#: 19523490 (see pubmed.gov for this free abstract only)