New Insights for Huntington's Disease Treatment

Dear Colleagues,

Huntington’s disease (HD) is a progressive neurodegenerative disorder with symptoms such as uncoordinated motor movement, emotional disturbance, and cognitive abnormality. The initial manifestation of HD occurs in midlife, and progressive decline after onset leads to inevitable fatality. More than 150 years after its initial clinical description by George Huntington, we know that HD is associated with numerous neuropathological changes. These changes include significant neuronal loss, astrogliosis, and gross degeneration of the caudate nucleus and the putamen. Moreover, the initial phase of HD has a greatest influence on medium spiny neurons (MSNs). This indicates a particular neuronal vulnerability and topographic susceptibility that is selectively patterned. Since the Huntington’s Disease Collaborative Research Group’s genetic investigation identified the HTT (huntingtin) gene (known as interesting transcript 15 on the chromosome 4) in 1993, many studies have determined the pathologic mechanisms of HTT in MSNs. However, a direct mechanism to explain the pathway from genetic mutation to neuronal atrophy has not yet been fully understood. Today, a growing body of evidence points toward epigenetic modification as being part of a fundamental molecular mechanism involved in HD pathogenesis. Even though HD is highly investigated, there is currently no applicable clinical treatment that can delay the onset or slow the disease progression of HD. Together, the key to discovering biological markers and therapeutics for the treatment of HD may potentially be possible through breakthrough research. In this context, this Special Issue of Cells invites research or review manuscripts on new insights for HD treatment and advanced neuropathological mechanisms of HD. The issue also invites manuscripts on AI platform-based therapeutic approaches in HD.

Prof. Dr. Hoon Ryu
Dr. Junghee Lee
Guest Editors

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• Huntington’s disease
• medium spiny neurons
• therapeutics
• neuropathology
• epigenetics
• non-cell autonomous pathway
• GABA
• dopamine
• chorea