"Gene Haywood" <gehayw at hotmail.com> wrote in message
news:bd56540c.0305252014.27f49b70 at posting.google.com...
> Where neurons are not killed outright, to what extent is neuronal
> damage caused by amphetamines reversible?
Interesting question. However, the main neurons damaged by amphetamines are
probably dopaminergic, and neurogenesis of these cells is probably very
limited if at all. Additionally, I have noted a study in the Journal of
Neurochemistry showing that dopaminergic neurons can be damaged and
dysfunctional but remain alive. This raises questions regarding typical
means of determining CNS damage from various agents. Recovery will be
contingent upon age, dietary status, general health, mtDNA damage a very
strong candidate for ongoing dysfunction as mtDNA much more suspectible to
ROS damage than nuclear DNA. Interestingly, EPA administration to aged rats
produced marked improvements in hippocampal LTP(probably via reduced
presence of il 1 which is strongly implicated in age associated cognitive
impairment and many others) and another study where alpha lipoic acid
(generates protective gene transcription) and acetyl l carnitine (improves
transport across mitochondrial membrane), also provided marked enhancement
of cognition in rats.
As to the studies showing mild short term amphetamine doses causing lasting
damage, I'm inclined to view these with suspicion. Remember all those peer
reviewed studies about the neurological horrors of marijuana? Turns out that
cannabinoids are amongst the most powerful neuroprotective agents
available(Hampson et al, PNAS, July 7, 1998) and a recent study by Fried
published in the Canadian Medical Journal claimed that post M use former
chronic light smokers had increased iq (5.8pts) and even ongoing light
smokers showing slightly higher iqs while current heavy smokers had slightly
reduced iq but upon cessation had slightly increased iq (2.1 I think).
Significantly, Fried did a series of longitudinal prospective studies on
children whose mothers smoked during pregnancy and established deficits in
these children, so he is hardly pushing the M barrow. However, another
longitudinal study by Solwicj and Hall in Aus found that the most
significant impairment from ongoing M smoking was in the academic realm ....
Confused? Join the club.
MDMA purportedly causes permanent serotonergic dysfunction but I have noted
studies in rats and one with women where after about 12 months the deficits
vanished. I vaguely recall some primate studies showing that serotonergic
neurons being replaced by news after loss. Sounds strange I know, but hey
until a few years ago we all thought there were no new brain cells in the
adult brain and now we're finding them in olfactory bulb, dentate gyrus,
spinal cord, and probably quite a few other places. The most startling
example I saw was a primate study which tracked the migration of new neurons
to damaged areas, this taking some two weeks.
In general it seems to depend on the individual, diet, genes, lifestyle, may
all play important roles in determining rate of recovery. Incidentally, the
famous mathematican, Paul Erdos, used a type of amphetamine for many years
and it didn't appear to do him any harm. On the other hand, if you've ever
seen speed psychosis, you soon have little doubt that serious damage has
occurred. As a general rule, amphetamines are very bloody dangerous when
used for extended periods or in heavy doses. Those bloody MAOs ... . Try L
In perspective, depression, chronic stress, also cause organic damage to the
brain. As does chronically low folate, omega 3's ... . I think if occasional
drug use was as dangerous as some would like us to believe then there'd be a
lot more sick puppies around. When looking at these studies, look very
carefully at the degree of deficit.