Nancy A. Jenkins

TL;DR: Transgenic mice that express a cDNA encoding an N-terminal fragment of huntingtin with 82, 44 or 18 glutamines develop behavioral abnormalities, including loss of coordination, tremors, hypokinesis and abnormal gait, before dying prematurely, consistent with the idea that N-Terminal fragments of Huntington's disease with a repeat expansion are toxic to neurons, and that N.terminal fragments are prone to form both intranuclear inclusions and neuritic aggregates.

TL;DR: Subcellular fractionation of LPS-stimulated macrophages revealed that LPS signals transduced by Tpl2 specifically promote the transport of TNF-α mRNA from the nucleus to the cytoplasm.

TL;DR: The first mutations in a mammalian central nervous system-specific voltage-sensitive calcium channel gene that is mutated in tg and tg(la) mice are defined and the first gene involved in absence epilepsy is identified.

TL;DR: The use of an improved expression cloning method is used to isolate human and murine cDNA clones encoding a second type of IL‐1 receptor (type II receptor), which appears to be well conserved in evolution and map to the same chromosomal location.

TL;DR: It is demonstrated that the A53T mutant α-synuclein causes significantly greater in vivo neurotoxicity as compared with other α-Syn variants, and α- synuclein-dependent neurodegeneration is associated with abnormal accumulation of detergent-insoluble α- Syn.