The pharmacodynamics of ReS9-S7, which concerns early stage research in possible toxicity [1]. The element being researched, alpha-synuclein, has never been shown to cause Parkinson's Disease, but instead has been found only to be affected as a result of it.

Exploring curcumin (which is found in a curry spice)  as a possible treatment of Parkinson's Disease [2]. Curcumin is already widely used, due to its ready availability, but has never rid Parkinson's Disease.

The effect of novel neuronal nicotinic receptor compounds on dyskinesia [3]. Smoking has the same effect on the nicotinic receptors due its nicotine contact, yet does not rid dyskinesia.

Assessment of the therapeutic efficacy of progranulin in a sub-chronic animal model of Parkinson’s disease [4]. Other researchers have already shown that progranulin has no potential in the treatment of  Parkinson's Disease.

Validation of LRRK2 as a drug target for treatment of Parkinson’s disease using antisense technology [5]. LRRK2 concerns only a genetic form of Parkinson's Disease.

Optimising lead series of small molecule inhibitors of LRRK2 to deliver tool compounds and clinical development candidates [6]. LRRK2 concerns only a genetic form of Parkinson's Disease.

A novel approach to characterize the distribution of a potentially therapeutic dominant-negative inhibitor of TNF in pre-clinical models of PD, and predict the scalability for an effective delivery of therapy in the human brain [7]. This aims for drugs to be able to by pass  the blood brain barrier. However, Parkinson's Disease has never been shown to be due to a deficiency of the blood brain barrier.

Pre-clinical development of a Parkinson’s disease therapy using a glucagon-like peptide (GLP-1) receptor agonist [8]. It is already approved by the FDA, but for diabetes rather than Parkinson's Disease.

Optimization of MOR antagonists for the treatment of L-DOPA-induced dyskinesias in Parkinson’s Disease [9]. The theory behind its use does not, even in theory, address the fact that dyskinesia is due to excessive L-dopa.

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