Alzheimer's disease (AD) is the most common progressive form of dementia in the elderly. Two major neuropathological hallmarks of AD include cerebral deposition of amyloidbeta protein (A) into plaques and blood vessels, and the presence of neurofibrillary tangles in brain. In addition, activated microglia and reactive astrocytes are often associated with plaques and tangles. Numerous other proteins are associated with plaques in human AD brain, including Apo E and ubiquitin. The amyloid precursor protein and its shorter fragment, A, are homologous between humans and non-human primates. Cerebral A deposition has been reported previously for rhesus monkeys, vervets, squirrel monkeys, marmosets, lemurs, cynomologous monkeys, chimpanzees, and orangutans. Here we report, for the first time, age-related neuropathological changes in cotton-top tamarins (CTT, Saguinus oedipus), an endangered non-human primate native to the rainforests of Colombia and Costa Rica. Typical lifespan is 13-14 years of age in the wild and 15-20؉ years in captivity. We performed detailed immunohistochemical analyses of A deposition and associated pathogenesis in archived brain sections from 36 tamarins ranging in age from 6-21 years. A plaque deposition was observed in 16 of the 20 oldest tamarins (Ͼ12 years). Plaques contained mainly A42, and in the oldest animals, were associated with reactive astrocytes, activated microglia, Apo E, and ubiquitin-positive dystrophic neurites, similar to human plaques. Vascular A was detected in 14 of the 20 aged tamarins; A42 preceded A40 deposition. Phospho-tau labeled dystrophic neurites and tangles, typically present in human AD, were absent in the tamarins. In conclusion, tamarins may represent a model of early AD pathology. 321
Background and Purpose-The benefit of carotid endarterectomy for preventing recurrent stroke is maximal when surgery is performed within 2 weeks after ischemic stroke or transient ischemic attack; the benefit is reduced when surgery is delayed Ͼ2 weeks and essentially lost if delayed Ͼ3 months. Guidelines recommend endarterectomy within 2 weeks poststroke/transient ischemic attack for patients with symptomatic carotid stenosis. This study examined time to endarterectomy at designated stroke centers as a measure of evidence-based best practices for stroke prevention. Methods-From the Registry of the Canadian Stroke Network, we identified all consecutive patients presenting with acute ischemic stroke or transient ischemic attack at 12 provincial stroke centers (Ontario, Canada, 2003 and selected those with unilateral symptomatic carotid stenosis of moderate (50% to 69%) or severe (70% to 99%) degree. Using linkages to administrative databases, we identified patients who underwent carotid endarterectomy within 6 months after the symptomatic event and calculated the time intervals between the index event and surgery. We compared the timing of surgery according to age, sex, degree of stenosis, index event, geographic region, and year. Logistic regression assessed variables associated with early surgery. Results-One hundred five patients underwent endarterectomy for unilateral symptomatic carotid stenosis (50% to 99%) within 6 months of the index event. The median time from index event to surgery was 30 days (interquartile range, 10 to 81). Only one third (38 of 105) received endarterectomy within the recommended 2-week target timeframe, and in one fourth (26 of 105), surgery was delayed Ͼ3 months. Surgery within 2 weeks was more likely if the index event was a transient ischemic attack rather than a stroke. Access to early endarterectomy varied markedly between hospitals across the province and improved over time from 2003 to 2006. Conclusions-In this hospital-based cohort, the majority of patients undergoing carotid endarterectomy after a transient ischemic attack or stroke had surgery delayed well beyond the period of maximum effectiveness. To enhance secondary stroke prevention, greater efforts are needed to minimize delays to diagnosis and surgical treatment for patients with symptomatic carotid stenosis.
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