Abstract: proposed that statins have supplementary possessions such


Treatment with
statins (3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors) decreases the
risk of ischemic stroke between patients with increased risk of vascular disease.
Current experimental abstracts point to neuroprotective properties of statins
in acute cerebral ischemia. There is an established fact in between
bioavailability of nitric oxide and the activity of statins and  ischemic stroke. On account of their
capability to up-regulate nitric oxide synthase, statins have been contemplated
in the therapy of a number of the central nervous system disorders, including
cerebral ischemia, Alzheimer’s disease, Parkinson’s disease, tumors, and
trauma. It has been asserted that they restrain inflammatory response and
secondary injury after acute ischemia.

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statins, Alzheimer’s disease, stroke,
multiple sclerosis, neuroprotection



have, at present, the promising ability to accommodate a new therapeutic goal
for multitudinal neurological diseases. It is well full-fledged that statins
decrease cholesterol levels and anticipate coronary heart disease. Moreover,
attestations proposed that statins have supplementary possessions such as
endothelial protection via action on the nitric oxide synthase system in
addition to antioxidant, anti-inflammatory and anti-platelet effects. These possessions
might have potential therapeutic association not only in stroke but also in neurological
disorders such as Alzheimer disease, Parkinson’s disease, multiple sclerosis
and primary brain tumors. The
principal mechanism of action of statins is based on the inhibition of
3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase and thus the
restriction of the enzyme in the biosynthesis of cholesterol. That results in
the growth in a number and activity of low density lipoprotein (LDL) receptors,
and decrease in this cholesterol fraction in the plasma as a consequence 1


Apart from cholesterol-dependent
mechanisms of action, statins also precisely up-regulate endothelial nitric oxide
synthase (eNOS, also titiled NOS3 or NOS III) expression, independent of
cholesterol levels 2, 3.





Statins decreases strokes
of various etiology by a array of mechanisms, containing modulation of
precerebral atherothrombosis in the aorta and the carotid artery and therefore
anticipating plaque division and artery-toartery thromboembolism by restricting
coagulation at its various levels, degenerating tissue factor, innovation of
prothrombin to thrombin activity 4.


Vaughan et al. 5
have shown in experimental models of ischemic stroke that statin therapy decreases
the size of brain infarct and ameliorate neurologic after effect by direct
up-regulation of brain endothelial NO synthase. Additional to that, the
anti-inflammatory actions of statins probably contribute to neuroprotection and
stroke prevention.


The Pravastatin
Lipids and Atherosclerosis in the Carotids II (PLACII) study also established a
cognent decline in carotid intimal-medial thickness in pravastatin-treated
patients. The impact of statin treatment on aortic atherosclerosis has not been
broadly analysed 5. Decrease in stroke incidence by statins like pravastatin,
simvastatin 6 and lovastatin were also accustomed in short-term clinical
studies 7.


In the experiment
conducted by The Large Prospective Studies Collaboration Group, there was no correlation
between cholesterol and stroke. However, they did not categorize between
ischemic and hemorrhagic stroke 8. Cucchiara et al. 8 have shown that the
opposing effects of cholesterol on ischemic versus hemorrhagic stroke risk may
confuse efforts to compare cholesterol levels with stroke except stroke type (
i.e. hemorrhagic vs. ischemic) is taken into account.


In the Cholesterol
and Recurrent Events (CARE) Trial, the pravastatin group had a 31% lower
incidenceof all strokes, even though again the incidence of lethal strokes was
about the same. Summarizing, there was no increase in the rate of hemorrhagic
stroke 9.


On Comparisons of
statins, Laufs et al. 10 have showed the results that eshtablish that
rosuvastatin is at least as effective as simvastatin and atorvastatin and
provided better protection than lovastatin and mevastatin in the mouse middle
cerebral artery (MCA) stroke model.