Electronic Stroke CarePath: Integrated Approach to Stroke Care.

We describe the development, implementation, and outcomes of the first 2 years of the Electronic Stroke CarePath, an initiative developed for management of ischemic stroke patients in an effort to improve efficiency and quality of care for patients. The CarePath consists of care pathways for ischemic stroke that are integrated within the electronic health record. Patient-reported outcomes are collected using an external software platform.

Centenarian middle cerebral artery occlusion treated with intra-arterial mechanical embolectomy.

Advanced age, arbitrarily defined as over 80 years, has been an exclusion criterion in many clinical trials for the treatment of acute ischemic stroke. The oldest person, to our knowledge, treated for acute ischemic stroke with intra-arterial therapy is presented and, importantly, this patient was excluded from intravenous tissue plasminogen activator due to an advanced age of 100 years and arrival in our emergency department within the 3-4.5 h time window.

Episodic-like memory deficits in the APPswe/PS1dE9 mouse model of Alzheimer's disease: relationships to beta-amyloid deposition and neurotransmitter abnormalities.

Transgenic mice made by crossing animals expressing mutant amyloid precursor protein (APPswe) to mutant presenilin 1 (PS1dE9) allow for incremental increases in Abeta42 production and provide a model of Alzheimer-type amyloidosis. Here, we examine cognition in 6- and 18-month old transgenic mice expressing APPswe and PS1dE9, alone and in combination. Spatial reference memory was assessed in a standard Morris Water Maze task followed by assessment of episodic-like memory in Repeated Reversal and Radial Water maze tasks.

Nuclear-targeting of mutant huntingtin fragments produces Huntington's disease-like phenotypes in transgenic mice.

Huntington's disease (HD) results from the expansion of a glutamine repeat near the N-terminus of huntingtin (htt). At post-mortem, neurons in the central nervous system of patients have been found to accumulate N-terminal fragments of mutant htt in nuclear and cytoplasmic inclusions. This pathology has been reproduced in transgenic mice expressing the first 171 amino acids of htt with 82 glutamines along with losses of motoric function, hypoactivity and abbreviated life-span.

Environmental, pharmacological, and genetic modulation of the HD phenotype in transgenic mice.

The HD-N171-82Q (line 81) mouse model of Huntington's disease (HD), expresses an N-terminal fragment of mutant huntingtin (htt), loses motor function, displays HD-related pathological features, and dies prematurely. In the present study, we compare the efficacy with which environmental, pharmacological, and genetic interventions ameliorate these abnormalities. As previously reported for the R6/2 mouse model of HD, housing mice in enriched environments improved the motor skills of N171-82Q mice.