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

TL;DR: The results suggest that occlusion of PKA-dependent processes is one of the molecular mechanisms underlying cognitive decline in R6 animals and that hippocampal PKA inhibition by infusion of Rp-cAMPS restored long-term memory in R 6/2 mice.

TL;DR: The idea of anatomical, electrophysiological and functional segregation within the perirhinal cortex itself and as part of a hippocampal-parahippocampal network is discussed and it is suggested that understanding this segregation is of critical importance in understanding the role and contributions made by the perireginal cortex in general.

TL;DR: While HD patient iPSCs can successfully differentiate toward a cortical fate in culture, the resulting neurons display altered transcriptomics, morphological and functional phenotypes indicative of altered corticogenesis in HD.

TL;DR: Reading literature evaluating the molecular, morphological, and physiological alterations in the cerebral cortex, a key component of brain circuitry controlling motor behavior, as they occur in both patients and transgenic HD models indicates that dysfunctional cortical input to the striatum sets the stage for the emergence of HD neurological signs.

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: These studies indicate that analyses of the caudate nucleus in grade 4 would reflect mainly its astrocytic composition with a component of remote neurons projecting to the striatum, which would reflect early cellular and biochemical changes in HD.

TL;DR: This work focuses on the central issue in this dispute — the relative contributions of the hippocampus and the perirhinal cortex to recognition memory.

TL;DR: These mice demonstrate that initial neuronal cytoplasmic toxicity is followed by cleavage of htt, nuclear translocation of htt N-terminal fragments, and selective neurodegeneration, clearly showing that aggregates are not essential to initiation of neuronal death.