"In contrast, when a person with dementia presents with only 'mild' effects on routine activities and cognitive function, fitness to drive should be determined on a caseby-case basis (Carmody et al. 2012). The importance of addressing fitness to drive for those with dementia has been defined in position statements published in Canada, USA, Australian and New Zealand (Lyketsos et al. 2006, Hogan et al. 2008). Hogan et al. (2008) outlined approaches to managing driving retirement in the Canadian Medical Association Journal including the family doctor's responsibility to monitor and counsel patients with progressive dementia who will eventually need to cease driving. "
"Considerable attention has been focused on the accumulation of β-amyloid peptide (Aβ) within the brain as a major etiologic factor in the pathogenesis of Alzheimer disease (AD). The commonly used drugs for AD like memantine, is a N-methyl-D-aspartic acid (NMDA) receptor antagonist, which may restore the functions of damaged neurons through reducing abnormal excitatory signals via the modulation of NMDA receptor activity  and cholinesterase (AChE) inhibitors suppress the enzymatic hydrolysis of neurotransmitter acetylcholine, thus maintain a higher acetylcholine concentration in the neuronal synapse , provide a symptomatic relief but no cure for the disease. At present, there is no curative treatment available for AD and the approved medications are used only for slowing the disease progression or providing prophylaxis. "
[Show abstract][Hide abstract] ABSTRACT: Alzheimer's disease (AD) is characterized by progressive dysfunction of memory and higher cognitive functions with abnormal accumulation of extracellular amyloid plaques and intracellular neurofibrillary tangles throughout cortical and limbic brain regions. At present no curative treatment is available, and research focuses on drugs for slowing disease progression or providing prophylaxis. Withania somnifera (WS) also known as 'ashwagandha' is used widely in Ayurvedic medicine as a nerve tonic and memory enhancer. However, there is a paucity of data on the potential neuroprotective effects of W.somnifera against β-Amyloid (1-42)-induced neuropathogenesis. In the present study, we have tested the neuroprotective effects of methanol:Chloroform (3:1) extract of ashwagandha against β-amyloid induced toxicity and HIV-1Ba-L (clade B) infection using a human neuronal SK-N-MC cell line. Our results showed that β-amyloid induced cytotoxic effects in SK-N-MC cells as shown by decreased cell growth when tested individually. Also, confocal microscopic analysis showed decreased spine density, loss of spines and decreased dendrite diameter, total dendrite and spine area in clade B infected SK-N-MC cells compared to uninfected cells. However, when ashwagandha was added to β-amyloid treated and HIV-1 infected samples, the toxic effects were neutralized. Further, the MTT cell viability assays and the peroxisome proliferator-activated receptor-γ (PPARγ) levels supported these observations indicating the neuroprotective effect of WS root extract against β-amyloid and HIV-1Ba-L (clade B) induced neuro-pathogenesis.
PLoS ONE 10/2013; 8(10):e77624. DOI:10.1371/journal.pone.0077624 · 3.23 Impact Factor
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