A YAC mouse model for Huntington's disease with full-length mutant huntingtin, cytoplasmic toxicity, and selective striatal neurodegeneration.

TL;DR: Expansions of CAG trinucleotide repeats coding for polyglutamine (polyQ) stretches have been found to be the causative mutation in at least eight hereditary neurodegenerative disorders, which include spinal and bulbar muscular atrophy and spinocerebellar ataxia type 7.

TL;DR: Two general hypotheses to explain why ampakines might have therapeutic value with regard to disparate psychiatric illnesses are described: one defining the machinery that reorganizes the spine cytoskeleton so as to encode memory and the other suggesting that defects in these same cellular processes contribute to a surprisingly large number of disorders involving memory and cognition.

TL;DR: This review will discuss neuroprotective gene therapies and restorative cell transplantation therapies that are in use for HD research and therapy.

TL;DR: In this article, the authors used haplotype analysis of linkage disequilibrium to spotlight a small segment of 4p16.3 as the likely location of the defect, which is expanded and unstable on HD chromosomes.

TL;DR: This article showed that chronic intraventricular infusion of D,L-AP5 causes a selective impairment of place learning, which is highly sensitive to hippocampal damage, without affecting visual discrimination learning.

TL;DR: Mice have been generated that are transgenic for the 5' end of the human HD gene carrying CAG/polyglutamine repeat expansion that exhibits many of the features of HD, including choreiform-like movements, involuntary stereotypic movements, tremor, and epileptic seizures.

TL;DR: An NH2-terminal fragment of mutant huntingtin was localized to neuronal intranuclear inclusions and dystrophic neurites in the HD cortex and striatum, and polyglutamine length influenced the extent of huntingtin accumulation in these structures.