Article
SK-PC-B70M alleviates neurologic symptoms in G93A-SOD1 amyotrophic lateral sclerosis mice.
Department of Brain & Cognitive Sciences, Ewha Womans University, Seoul, 120-750, Republic of Korea.
Brain research (impact factor:
2.46).
10/2010;
1368:299-307.
DOI:10.1016/j.brainres.2010.10.048
pp.299-307
Source: PubMed
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Citations (0)
- Cited In (3)
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[show abstract] [hide abstract]
ABSTRACT: Cognitive enhancers (nootropics) are drugs to treat cognition deficits in patients suffering from Alzheimer's disease, schizophrenia, stroke, attention deficit hyperactivity disorder, or aging. Cognition refers to a capacity for information processing, applying knowledge, and changing preferences. It involves memory, attention, executive functions, perception, language, and psychomotor functions. The term nootropics was coined in 1972 when memory enhancing properties of piracetam were observed in clinical trials. In the meantime, hundreds of drugs have been evaluated in clinical trials or in preclinical experiments. To classify the compounds, a concept is proposed assigning drugs to 19 categories according to their mechanism(s) of action, in particular drugs interacting with receptors, enzymes, ion channels, nerve growth factors, re-uptake transporters, antioxidants, metal chelators, and disease modifying drugs meaning small molecules, vaccines, and monoclonal antibodies interacting with amyloid-β and tau. For drugs whose mechanism of action is not known, they are either classified according to structure, e.g., peptides, or their origin, e.g., natural products. This review covers the evolution of research in this field over the last 25 years.Journal of Alzheimer's disease: JAD 10/2012; · 3.74 Impact Factor
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Keywords
active ingredient(s)
age attenuated neurological deficits
amyotrophic lateral sclerosis
anti-choline acetyltransferase
cresyl violet
cytotoxicity induced
G93A-SOD1 ALS mice
G93A-SOD1 mice
G93A-SOD1 transgenic mouse model
helpful effects
histologic analysis stained
neurologic deficits
oleanolic-glycoside saponins fraction
plaque deposition
Pulsatilla koreana
scopolamine-induced deficits
SK-PC-B70M affords
SK-PC-B70M suppressed neuronal loss
spinal cord
Tg2576 mouse model