[/quote]
Regarding reduced glucose consumption - it's actually often a good thing. Reduced glucose consumption is often an indicator of efficiency. In fact, the brain regions of smarter people require less glucose to perform the same task, as compared to those of dumber people. See
http://www.sciencedi...191886994900493[/quote]
I like that link. Here is an interesting quote from a recent article. About transplantation of brain cells. I am interested in the effects of amphetamines on schwann cells and oligodendrocytes atm which make up myelin which in turn have ramafications on intelligence.
[quote]Abstract
Cell replacement therapy has been proposed as a means to replace lost dopaminergic neurons in Parkinson's disease (PD). In most studies, the transplanted cells have been placed within the target site, the striatum, and not within the lesioned site, the substantia nigra, as the adult nigrostriatal pathway was thought to constitute a non-permissive environment for long distance axonal outgrowth of transplanted neuroblasts. Here, we discuss recent findings showing that intranigral transplanted dopaminergic neuroblasts can form axonal projections to the striatum, resulting in increased striatal dopamine levels and ameliorating behavioral deficits in animal models of PD. Such findings have raised new hopes and opened new avenues for cell replacement therapy in patients with PD.
[/quote]
Also
this patent to deal with neurotoxicity is recent and fascinating. I will have to look into it later on it may come in tablet form.
This next study is interesting. It basically says that young rats with neurotoxity or whatever derived brain lesions profit about 100% from transplanted cells and then the efficacy goes down to 50% in the middle aged and then 0% in the old. So, the lesson is if you suspect any kind of brain damage it is best to treat it immediately, at least for rats.
[quote]We examined the behavioral and morphological correlates of
the response to a single intrastriatal dispersed cell graft of fetal
rat ventral mesencephalic tissue in male Fischer-344 rats of
varying age (4, 17, and 24–26 months old) and history of
mesostriatal dopamine (DA) depletion (1 or 14 months). Our
goal was to determine the impact of advancing age and duration
of DA depletion in the host on DA graft viability and
function. The findings can be summarized as follows. (1) Fetal
DA neuron grafts that were effective in completely ameliorating
amphetamine-induced rotational behavior in young rats with
short-term lesions were virtually without effect in aged rats with
long-term lesions. Middle-aged rats with long-term lesions responded
to these grafts with partial behavioral recovery. (2) Age
of the host at the time of transplantation, and not duration of DA
depletion, was the primary determinant of response to DA
grafts. (3) Diminished efficacy of grafts in lesioned aging rats
was related to decreased survival and neurite extension of
transplanted DA neurons. (4) Co-grafts of DA neurons with
Schwann cells as a source of neurotrophic support improved
the behavioral outcome of grafts in aged lesioned rats. These
findings support the view that the DA-depleted striatum of aged
rats is an impoverished environment for survival, growth, and
function of DA grafts. Consistent with this view, local supplementation
of the neurotrophic environment of grafted DA neurons
with products of co-grafted Schwann cells, a demonstrated
source of neurotrophic activity for embryonic DA
neurons, improved graft outcome.[/quote]
This quote deals with METH not necessarily amphetamine but it does cause destruction of the myelin via destruction of oligodendrocites which make up the myelin along side schwann cells. I am not sure if amphetamine will do the same via the mRNA expression. Why do these cells decide to kill themselves in the presence of this molecule, puzzling? There is a paper on the nature of neurotoxins that I need to read perhaps that will shed some light. There are also apoptosis inhibitors, but I don't know how those would work yet. The above metioned patent probably work along those lines.
[quote]Abstract
We investigated whether the psychostimulant methamphetamine (METH) has a cytotoxic effect on oligodendrocytes and which cell-death pathways are involved in the cytotoxic process. METH caused concentration- and time-dependent cytotoxicity in rat oligodendrocyte cultures. METH induced apoptotic cell death and mRNA expression of pro-apoptotic proteins (bax and DP5), but not anti-apoptotic proteins (bcl-2 and bcl-XL). These results suggest that
METH induces cytotoxicity in rat oligodendrocytes via the differential regulation of the expression of genes involved in the apoptotic process.[/quote]
The last thing I am looking into is the fact that BDNF is excreted from oligodendrocytes so they are very important cells and this is regulated by glutamate which also regulates apoptosis IIRC. I also want to know the differences if any from rat glial cells and that of humans if any.
