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Use of specific inhibitors of stress-activated protein kinases to preserve fast axonal transport function in the treatment of polyglutamine expansion neurodegenerative diseases

Therapeutic
Therapeutic

The polyglutamine expansion diseases include Kennedy’s Disease (Spinobulbar muscular atrophy), Huntington's disease (HD), and several spinocerebellar ataxias (SCAs). Remarkably, each is caused by CAG codon expansion within a particular gene that produces polyglutamine tract enlargement in the protein. Each such mutant protein causes selective neurodegeneration within the CNS. Formation of nuclear and cytoplasmic aggregates that include such mutant proteins is a characteristic feature of polyglutamine expansion diseases in patients as well as transgenic animal and cell culture models. The precise role of these protein aggregates in pathogenesis remains uncertain.

Description/Details

The researchers at UIC have identified a molecular mechanism of pathogenesis in polyglutamine expansion diseases that leads to neurodegeneration. Based on their studies on the pathogenesis of the diseases, they have found that the inappropriate activation of specific kinases (one or more members of the stress activated protein kinase family - SAPK) are responsible for the neurodegeneration. Such activation leads to a significant reduction in the normal trafficking of membrane-bounded organelles mediated by microtubule based motors. In order to treat affected neurons, the researchers propose using specific SAPK inhibitors to treat the neurons undergoing the neurodegenerative changes seen in polyglutamine expansion diseases. The technique will prevent neurodegeneration and maintain neuronal function in affected patients.

Applications

Therapeutic: Applicable for the development of new and effective treatments for polyglutamine expansion diseases, Research: Applicable for pharmaceutical companies or academia interested in neurodegenerative disease research

Benefits

The proposed treatment is expected to halt or dramatically slow the progression of the polyglutamine expansion diseases, The mechanism of action that leads to neurodegeneration in these diseases is known, The treatment is target specific, The treatment targets an early event in pathogenesis specific to these diseases

Reference #

CY035
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