Abnormal cortical synaptic plasticity in a mouse model of Huntington's disease.

TL;DR: Altered excitatory and inhibitory inputs to pyramidal neurons in the cortex in HD appear to be a prevailing deficit throughout the development of the disease.

TL;DR: An overview of the neurochemical mediators and modulators of synaptic transmission that are disrupted in HD will provide an overview of classical neurotransmitters like glutamate and gamma‐aminobutyric acid, modulators such as dopamine, adenosine and endocannabinoids, and molecules like brain‐derived neurotrophic factor which affect neurotransmission in a more indirect manner.

TL;DR: Neurochemical, electrophysiological, and behavioral studies in HD patients and genetic mouse models suggest biphasic changes in DA neurotransmission, and targeting both DA and glutamate receptor dysfunction could be the best strategy to treat HD symptoms.

TL;DR: These findings demonstrate multiple perturbations to corticostriatal synaptic function in HD mice, furthering the understanding of the early effects of the HD mutation that may contribute to cognitive dysfunction, mood disorders and later development of more serious dysfunction.

TL;DR: The age of onset of symptoms is extraordinarily inconsistent as discussed by the authors and most individuals first develop symptoms between the ages of 30 and 40 years, although symptoms can occur between 20 and 60, a span of four decades.

TL;DR: It is suggested that HD patients' functional deficits do not evolve uniformly, and performance on psychomotor tasks in people with the mutation who were close to clinical onset of HD was intermediate between that of individuals many years from onset and those in the early stages of HD, suggesting a slowly insidious evolution of deficit.

TL;DR: A brief overview of the importance of standardizing the use of HD mice is provided and brief protocols used for genotyping the mouse models used within the Bates Laboratory are described.