Re: Performance enhancement with selegiline

From: Rafal Smigrodzki (rms2g@virginia.edu)
Date: Sat Feb 08 2003 - 18:26:28 MST

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    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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