Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this study, we immunohistochemically examined the several constituents of senile plaques (SPs) and cerebral amyloid angiopathy (CAA) in aged cynomolgus monkeys. Apolipoprotein E (apoE) deposited in all mature plaques and CAA, and in half of the diffuse plaques. Alpha-1-antichymotripsin (alpha ACT) deposited in half of the mature plaques and in one third of the CAA. Amyloid precursor protein (APP), ubiquitin (Ub), and microtubule-associated protein-2 (MAP-2) accumulated in the swollen neurites of mature plaques. Glial fibrillary acidic protein (GFAP) was detected in the astrocytes and their processes surrounding the mature plaques. Tau was detected in neither the SPs nor CAA. Therefore, mature plaques involved extracellular A beta, apoE, and alpha ACT, and also astrocytes and swollen neurites. However, diffuse plaques involved only extracellular A beta and apoE. Since these features, except for tau, were consistent with those in humans, this animal model will be useful for studying the pathogenesis of cerebral amyloid deposition.
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PMID:Immunohistochemical characteristics of the constituents of senile plaques and amyloid angiopathy in aged cynomolgus monkeys. 890 9

The aims of neurology in Japan in the 21st Century should include establishment of therapeutic measures for neurological diseases, training clinical neurologists to cover both static and dynamic aspects of neurology, and application of gene therapy and neurogenesis to clinical neurology. It is also important to note that once any neurological disease develops, remaining sequelae are usually not curable, so the problem of how to prevent the onset of neurological diseases, that is preventive neurology, will become increasingly important. The key target for prevention in neurology is cerebro-vascular disease, since it is very common. Many risk factors are known for ischemic CVD. However, even for the management of hypertension, the so-called number needed to treat (NNT) is 29-118/5 years for primary prevention and 14-23/5 years for secondary prevention. It is also important to consider genetic factors that influence CVD, including abnormal plasminogen, Lp (a), ACT Isehara 1 gene, apolipoprotein E and so on, since these congenital factors reinforce known acquired risk factors, such as hypertension. In addition, the presence of asymptomatic cerebral infarction, as well as PVH and DSWMH, in MRI T2-weighted images is an important predictor of future symptomatic CVD. Finally, storage of one's own bone marrow cells might be useful, since in the event of onset of CVD, dementia or other neurological diseases, autotransplantation with cytokine might become available for neurogenesis. The results of our recent experiments indicate that this idea may be feasible.
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PMID:[Neurology in the 21st century--the era of preventive neurology utilizing new diagnostic and therapeutic techniques]. 1515 50