From: Rafal Smigrodzki (rms2g@virginia.edu)
Date: Sat Feb 08 2003 - 18:26:28 MST
I know of at least five compounds (calcium blockers, iron chelators, and
other things I already forgot about) that worked in the same model, but
failed in clinical trials. The Stroke Institute in Pittsburgh is always
running two-three trials simultaneously, but so far nothing panned out.
Rafal
----- Original Message -----
From: "gts" <gts_2000@yahoo.com>
To: "gts" <gts_2000@yahoo.com>; <extropians@extropy.org>
Sent: Saturday, February 08, 2003 6:47 AM
Subject: Re: Performance enhancement with selegiline
> Here is more evidence of neuroprotection by selegiline/deprenyl:
>
> This is evidence that selegiline protects neurons from death due to from
> temporary lack of oxygen (hypoxia) as in stroke (ischemia).
>
> ABSTRACT
> L-deprenyl reduces brain damage in rats exposed to transient
> hypoxia-ischemia.
>
> Stroke 1995 Oct;26(10):1883-7 (ISSN: 0039-2499)
> Knollema S; Aukema W; Hom H; Korf J; ter Horst GJ
> University of Groningen, Department of Biological Psychiatry, The
> Netherlands.
> BACKGROUND AND PURPOSE: L-Deprenyl (Selegiline) protects animal brains
> against toxic substances such as 1-methyl-1,2,3,6-tetrahydropyridine and
> 6-hydroxydopamine. Experiments were conducted to test whether L-deprenyl
> prevents or reduces cerebral damage in a transient hypoxia/ischemia rat
> model. METHODS: Rats were treated for 14 days with 2 mg/kg and 10 mg/kg
> L-deprenyl or saline. After surgery a 20-minute hypoxia/ischemia period
was
> induced by simultaneous occlusion of the left common carotid artery and
> reduction of the percentage of oxygen in the gas mixture to 10%. Rats were
> killed 24 hours later. Silver staining was used to reveal damage in
several
> brain regions. RESULTS: In the brain, both L-deprenyl dosages reduced
damage
> up to 78% compared with the controls. Total brain damage was decreased
from
> 23%-31% to 5%-9% with the L-deprenyl treatment (2 mg/kg: F1.13 = 6.956, P
<
> .05; 10 mg/kg: F1.13 = 5.731, P < .05). In the striatum, significant
> treatment effects were found between both the L-deprenyl groups (2 mg/kg
and
> 10 mg/kg, respectively) and the saline group (F1.13 = 14.870, P < .005;
and
> F1.13 = 8.937, P = .01; respectively). In the thalamus, significant
> treatment effects were seen in the 2-mg/kg L-deprenyl group (F1.13 =
11.638,
> P < .005) and the 10-mg/kg group (F1.13 = 8.347, P < .05) compared with
the
> control group. No significant damage decrease was seen in the hippocampus
> and the cortex. CONCLUSIONS: The results show that L-deprenyl is effective
> as a prophylactic treatment for brain tissue when it is administered
before
> hypoxia/ischemia. Mechanisms responsible for the observed protection
remain
> unclear. The regional differences in damage, however, are in accordance
with
> the reported regional increase in superoxide dismutase and catalase
> activities after L-deprenyl treatment, suggesting the involvement of free
> radicals and scavenger enzymes.
>
>
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