Dear,

To my knowledge there are only 2 experimental treatments for alpha-synucleinopathies in clinical trials: where one is a vaccine developped by Affiris (Phase 1) and the other is a small molecule from the NIH called Phenserine (Phase 2). All others are currently in Discovery stage.

By the way the Michael Jay Fox Foundation is doing a lot in order to help patients as well as supporting the developpement of novel treatments to treat Parkinson's disease

Experiments to test neuroprotective efficacy of RAB3B in pre-clinical models of alpha-synucleinopathy is under way (https://www.michaeljfox.org/foundation/grant-detail.php?grant_id=724). In addition, Parkin gene therapy has been suggested to be effective against alpha-synucleinopathy (Hum Gene Ther. 2005 Feb;16(2):262-70 and Expert Rev Neurother. 2007 Aug;7(8):957-60).

An in-depth overview on the role of alpha-synuclein in neurodegeneration (including Parkinson's disease) recently appeared at:

http://www.springerlink.com/content/j541402612570666/fulltext.pdf?MUD=MP (free download).

NO. Pharmacotherapy of central nervous system is depend on the dysregulations of neurotransmitters.

Therefore, I do not consider the alpha-synucleinopath.

Dr Prusiner, who was the originator of the prion infectous protein hypothesis just published an intersting perspective in Science (Prusiner, Science 336:1511-13, June 22 2012) which discusses recent findings extending the role of prions from BSE/vCJD to other neurogenerative diseases like Alzheimer's and Parkinson's disease and how this can lead to novel drug target strategies

Inhibition of alpha-synuclein aggregation is expected to be counteracted by extracellular chaperons such as Haptoglobin. This protein, in the CNS, is secreted by activated astrocytes, and was demonstrated to inhibit amyloid aggregation in vitro. No Haptoglobin-mimetic peptide has been studied for inhibting alpha-synuclein aggregation to date.

Reply from Lueder Deecke: Basically the answer No would be correct. However, there is a Parkin gene therapy in the literature, but as far as I see we are on the level of a rat model only. My other suggestion is a clinical experience statement. It is worth trying Rasagilin (Azilect), which in my opinion is really effective in slowing down the progression rate of Parkinson's disease. Best!

alpha synuclein may be a sure merkmar for Parkinson's disease. But treatment of the molecule may not be clear for development of the disease. Rather, you might be better to find the molecule as a marker for diagnosing the disease.

Strictly speaking there are many "experimental" treatments for synucleopathy in PD, that is to say:

many in pre-clinical models, some in clinical trials - none however in clinical practice.

I have to mention here reMYND (Leuven, Belgium)

who have a small compound that is about to enter phase 1

http://www.remynd.com/drug_discovery/products_in_pipeline

It should be emphasized that α-synuclein (α-syn) was first found in association with amyloid plaques several years prior to its linkage to Lewy body formation/ Parkinson's disease. Undoubtedly, new therapies are urgently needed that modify, delay the onset, and/or attenuate progression of the disease – be it AD or PD. Aβ 42/Amyloid plaques correlate poorly with memory decline, since cognitively normal elderly also possess amyloid deposition and efforts at amyloid removal via immunotherapy have been unsuccessful in preventing progressive neurodegeneration, both in some animal models and the humans. Aβ and α-syn are proteins, possessing an inherent property of aggregation; they are typically associated with two distinct neurodegenerative disorders – viz. AD and PD respectively. However, they are also interesting proteins, in that Aβ, tau, and α-syn might promote the accumulation/aggregation of each another, both in vivo, in vitro, and indeed in the cell culture system. In terms of similarity between these two proteins, Aβ-induced upregulation of pro-inflammatory cytokines may activate cyclin-dependent kinase 5, and the latter is implicated in Lewy body formation as well as influencing α-syn aggregation also. We are aware of the results of amyloid clinical trials – we obviously wait anxiously of the results of trials, in respect of α-synuclein, that are meant to ameliorate PD.