Huntington’s disease is a hereditary neurodegenerative disorder with a fatal outcome. Despite the discovery of the genetic mutation 39 years ago, no effective treatment to date has emerged, which, in part, is related to the disease complexity. The development of transgenic models has unveiled many pathologic processes caused by the mutant huntingtin gene, ranging from disruption in gene transcription to impaired neurotransmission, which in some cases appears at the developmental stage and in others leads to compensatory mechanisms in adulthood. However, the treatment options available today only relieve some symptoms; no curable treatment has yet emerged.
This Research Topic aims to bring together new insights into Huntington’s disease neuropathology from preclinical to clinical research. Particularly, those that focused on the identification of therapeutic targets and future treatments.
The huntingtin protein, ubiquitously expressed throughout the body, is involved in several key molecular and cellular mechanisms. Therefore, its mutation in Huntington’s disease impacts genetic, molecular, and cellular functions, compromising communication between neurons and astrocytes, leading to abnormal behavioral changes. The Topic will provide an update on Huntington’s disease neuropathology to pave the way for the identification of potentially novel treatment targets.
This Research Topic will explore an update on the neuropathological insights elicited by mutant huntingtin from synapses to circuits. We welcome reviews, mini-reviews, and original research that cover the following Huntington’s disease (HD) topics:
- Cortical, cortico-striatal, cortico-striato-thalamic neuropathology in HD
- Dysfunction in glia and microglia
- Changes in neuron-astrocyte communication
- Neuroinflammation and HD
- Recent advances in therapeutic targets
- Oxidative damage
- Electrophysiological alterations in vitro and in vivo
- Relevant pathological changes in peripheral systems that might contribute to HD neuropathology (i.e. peripheral inflammation, microbiota, etc.)
Huntington’s disease is a hereditary neurodegenerative disorder with a fatal outcome. Despite the discovery of the genetic mutation 39 years ago, no effective treatment to date has emerged, which, in part, is related to the disease complexity. The development of transgenic models has unveiled many pathologic processes caused by the mutant huntingtin gene, ranging from disruption in gene transcription to impaired neurotransmission, which in some cases appears at the developmental stage and in others leads to compensatory mechanisms in adulthood. However, the treatment options available today only relieve some symptoms; no curable treatment has yet emerged.
This Research Topic aims to bring together new insights into Huntington’s disease neuropathology from preclinical to clinical research. Particularly, those that focused on the identification of therapeutic targets and future treatments.
The huntingtin protein, ubiquitously expressed throughout the body, is involved in several key molecular and cellular mechanisms. Therefore, its mutation in Huntington’s disease impacts genetic, molecular, and cellular functions, compromising communication between neurons and astrocytes, leading to abnormal behavioral changes. The Topic will provide an update on Huntington’s disease neuropathology to pave the way for the identification of potentially novel treatment targets.
This Research Topic will explore an update on the neuropathological insights elicited by mutant huntingtin from synapses to circuits. We welcome reviews, mini-reviews, and original research that cover the following Huntington’s disease (HD) topics:
- Cortical, cortico-striatal, cortico-striato-thalamic neuropathology in HD
- Dysfunction in glia and microglia
- Changes in neuron-astrocyte communication
- Neuroinflammation and HD
- Recent advances in therapeutic targets
- Oxidative damage
- Electrophysiological alterations in vitro and in vivo
- Relevant pathological changes in peripheral systems that might contribute to HD neuropathology (i.e. peripheral inflammation, microbiota, etc.)
