Parkinson’s Disease

Pathology and Physiology Overview

Parkinson’s disease (PD), a neurodegenerative movement disorder that can also cause dementia and behavioral abnormalities is another important disease target for NE3107.  PD and AD share many similarities with regard to the central roles of inflammation and insulin resistance on disease processes, although the diseases predominately attack different parts of the brain. 

Like Alzheimer’s disease, PD progresses slowly, with worsening symptoms resulting in disability five to ten years after diagnosis.  Most PD patients are treated with levodopa in combination with carbidopa that slows L-dopa metabolism to a form that cannot be transported into the brain (dopamine).  Prolonged use of L-dopa frequently causes a side effect of involuntary movements called L-dopa induced dyskinesia (LID), which can be as disabling as PD itself and is a major limitation to L-dopa therapy.

In PD the protein alpha synuclein (SNA) is over expressed and misfolded, which creates inflammatory SNA aggregates in a region of the brain called the substantia nigra that makes the movement mediating neurotransmitter, dopamine.  Inflammation causes neuron death and dysfunction in the substantia nigra and surrounding regions of the striatum (region of brain coordinating motion, decision making and other important functions), leading to a shortage of dopamine and suboptimal activity of the lower concentration of dopamine present because of neuron death.  NE3107 decreases neuroinflammation and the resulting insulin resistance to slow neurodegeneration and improve neuron function.

NE3107 reduced inflammation and enhanced insulin sensitivity in animal models, both of which have been shown to reduce PD pathology

Studies in a marmoset (a small new-world monkey) model of Parkinson’s disease demonstrated NE3107’s ability to decrease movement abnormalities that are the clinical signs of the disease. In the same study, NE3107 in combination with levodopa had a stronger effect on the disease than either drug alone, while monkeys treated with NE3107 developed less L-dopa induced dyskesia. NE3107 also had a strong neuroprotective activity that promoted the survival of twice as many neurons in the substantia nigra as monkeys treated with placebo.

Based on these initial results, BioVie plans to advance our clinical programs in Parkinson's.

Forward Looking Statements
This website contains forward-looking statements made pursuant to the safe harbor provisions of the Private Securities Litigation Reform Act of 1995 that involve risks, uncertainties, and assumptions that could cause BioVie’s actual results and experience to differ materially from anticipated results and expectations expressed in these forward-looking statements.
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