I love my Brain Sprouts I feed them daily some Brain Tonic that is full of "neurotrophic growth factors".

"Numerous neurotrophic growth factors help determine which neurons develop in the immature brain and which are retained in the adult brain. Neurotrophic factors can also induce neurons to sprout axons capable of growing into new locations and forming new synaptic connections, a process that continues in the mature brain."


http://www.psychiatrist.com/pcc/brainstorm/br5904.htm (main article)

http://www.psychiatrist.com/pcc/brainstorm/br5906.htm (therapeutic potential)

http://www.psychiatrist.com/pcc/brainstorm/br5806.htm (Glutamate assassin/excitotoxic neuron murder)

The Second Stage of MS is "The Degererative Stage" in which "excess Glutamate" runs wild on a killing spree. First phase, of course, is the "Inflammatory Stage".

http://home.ix.netcom.com/~jdalton/ms-two-stages.pdf

http://home.ix.netcom.com/~jdalton/two%20stage%20MS.jpg

Braindead

p.s Other good info here also:

http://www.psychiatrist.com/pcc/brainstorm/

Hey Jack, long time no see. Welcome back.
I've missed your posts.

Do you really believe in this brain food? Any
bad sides? Is it working for you? Which Brain
Tonic is the best?

How have you been.

One of the KEY "neurotrophic growth factors" is a substance called NERVE GROWTH FACTOR - NGF.

This is probably the single most practical ingredient in any contemporary "Brain Tonic" that one could take.

The problem with NGF when taken orally is that it does not make it through the BBB Blood Brain Barrier. Drilling a hole in the Brain and literally pouring some in does work, but has some practical limitations.

However NGF is GREAT for those small Brain repair jobs. (pun intended)

But it is not hopeless because some "things" that make it through the BBB can cause the Brain to make more NGF itself.

One of these substances is well known to MS folks - Vitamin D3. So it is a good idea to take plenty -year round!

Braindead

1: Neurosci Lett. 2003 Jun 5;343(2):139-43.

1,25-dihydroxy (vitamin D3) induces nerve growth factor, promotes neurite outgrowth and inhibits mitosis in embryonic rat hippocampal neurons.Brown J, Bianco JI, McGrath JJ, Eyles DW.
School of Biomedical Sciences, University of Queensland, Brisbane, Qld 4072, Australia.

There is an accumulation of evidence implicating a role for vitamin D(3) in the developing brain. The receptor for this seco-steroid is expressed in both neurons and glial cells, it induces nerve growth factor (NGF) and it is a potent inhibitor of mitosis and promoter of differentiation in numerous cells.

We have therefore assessed the direct effect of vitamin D(3) on mitosis, neurite outgrowth, as well as NGF production as a possible mediator of those effects, in developing neurons. Using cultured embryonic hippocampal cells and explants we found the addition of vitamin D(3) significantly decreases the percentage of cultured hippocampal cells undergoing mitosis in conjunction with increases in both neurite outgrowth and NGF production.

The role of vitamin D(3) during brain development warrants closer scrutiny.

PMID: 12759183 [PubMed - indexed for MEDLINE]

1: Behav Brain Res. 1997 Feb;83(1-2):117-22.Links
Orally active NGF synthesis stimulators: potential therapeutic agents in Alzheimer's disease.Yamada K, Nitta A, Hasegawa T, Fuji K, Hiramatsu M, Kameyama T, Furukawa Y, Hayashi K, Nabeshima T.
Department of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University School of Medicine, Japan.

The degeneration of cholinergic neurons may be responsible for cognitive impairment in patients with Alzheimer's disease (AD). Since nerve growth factor (NGF) plays an important role in the survival and maintenance of cholinergic neurons in the central nervous system, this factor may have some beneficial effects on the cognitive impairment observed in patients with AD. However, since NGF does not cross the blood-brain barrier and is easily metabolized when administered peripherally, it can only be used when directly injected into the brain. In this review, we show that repeated oral administration of the NGF synthesis stimulators, idebenone and propentofylline, partially restored the age-associated decrease of NGF in the frontal and parietal cortices. Furthermore, this treatment attenuated the impairment of performance in the water maze, passive avoidance, and habituation tasks in rats with bilateral forebrain lesions, and in rats which had received continuous infusion of anti-NGF antibody into the septum. The behavioral improvement induced by idebenone and propentofylline was accompanied by recovery of both the reduced activity of choline acetyltransferase and the changes in [3H]QNB binding. These results suggest that the use of NGF synthesis stimulators may provide a novel therapeutic approach to cholinergic dysfunction.

PMID: 9062669 [PubMed - indexed for MEDLINE]



1: Expert Opin Investig Drugs. 2000 Apr;9(4):747-64. Links
Apoptosis modulators in the therapy of neurodegenerative diseases.Deigner HP, Haberkorn U, Kinscherf R.
Anatomy and Cell Biology III University of Heidelberg, Germany.

Apoptosis is a prerequisite to model the developing nervous system. However, an increased rate of cell death in the adult nervous system underlies neurodegenerative disease and is a hallmark of multiple sclerosis (MS) Alzheimer's- (AD), Parkinson- (PD), or Huntington's disease (HD). Cell surface receptors (e.g., CD95/APO-1/Fas; TNF receptor) and their ligands (CD95-L; TNF) as well as evolutionarily conserved mechanisms involving proteases, mitochondrial factors (e.g. , Bcl-2-related proteins, reactive oxygen species, mitochondrial membrane potential, opening of the permeability transition pore) or p53 participate in the modulation and execution of cell death. Effectors comprise oxidative stress, inflammatory processes, calcium toxicity and survival factor deficiency. Therapeutic agents are being developed to interfere with these events, thus conferring the potential to be neuroprotective. In this context, drugs with anti-oxidative properties, e.g., flupirtine, N-acetylcysteine, idebenone, melatonin, but also novel dopamine agonists (ropinirole and pramipexole) have been shown to protect neuronal cells from apoptosis and thus have been suggested for treating neurodegenerative disorders like AD or PD. Other agents like non-steroidal anti-inflammatory drugs (NSAIDs) partly inhibit cyclooxygenase (COX) expression, as well as having a positive influence on the clinical expression of AD. Distinct cytokines, growth factors and related drug candidates, e.g., nerve growth factor (NGF), or members of the transforming growth factor-beta (TGF-beta ) superfamily, like growth and differentiation factor 5 (GDF-5), are shown to protect tyrosine hydroxylase or dopaminergic neurones from apoptosis. Furthermore, peptidergic cerebrolysin has been found to support the survival of neurones in vitro and in vivo. Treatment with protease inhibitors are suggested as potential targets to prevent DNA fragmentation in dopaminergic neurones of PD patients. Finally, CRIB (cellular replacement by immunoisolatory biocapsule) is an auspicious gene therapeutical approach for human NGF secretion, which has been shown to protect cholinergic neurones from cell death when implanted in the brain. This review summarises and evaluates novel aspects of anti-apoptotic concepts and pharmacological intervention including gene therapeutical approaches currently being proposed or utilised to treat neurodegenerative diseases.

PMID: 11060707 [PubMed - indexed for MEDLINE]
__________________

Folks you had better hurry-- the SALE on my "Brain Tonic" will be over in a few days!!!

Braindead

1: Prog Brain Res. 2004;146:403-14.

Role of nerve growth factor and other trophic factors in brain inflammation.

Villoslada P, Genain CP.

Neuroimmunology Laboratory, Department of Neurology, University of Navarra,
Spain.

Inflammation in the brain is a double-edged process that may be beneficial in
promoting homeostasis and repair, but can also result in tissue injury through
the damaging potential of inflammatory mediators. Thus, control mechanisms that
minimize the extent of the inflammatory reaction are necessary in order to help
preserve brain architecture and restore function.

The expression of neurotrophic factors such as nerve growth factor (NGF) is increased after brain injury, in part mediated by effects on astrocytes of pro-inflammatory mediators and cytokines produced by immune cells. Conversely, cells of the immune system express NGF receptors, and NGF signaling modulates immune function.

Multiple Sclerosis (MS) and the disease model experimental autoimmune encephalomyelitis are neurodegenerative disorders whereby chronic destruction of the brain parenchyma results from an autoaggressive, immune-mediated inflammatory process and insufficient tissue regeneration. Here, we review evidence indicating that the increased production of NGF and other trophic factors in central nervous system (CNS) during these diseases can suppress inflammation by switching the immune response to an anti-inflammatory, suppressive mode in a brain-specific environment.

Thus, trophic factors networks in the adult CNS not only protects
axons and myelin but appear to also actively contribute to the maintenance of
the brain immune privilege. These agents may represent good targets for
therapeutic intervention in MS and other chronic CNS inflammatory diseases.

PMID: 14699976 [PubMed - in process]

1: Iran J Allergy Asthma Immunol. 2006 Dec;5(4):177-81.

Nerve growth factor prevents demyelination, cell death and progression of the disease in experimental allergic encephalomyelitis.

Parvaneh Tafreshi A.
Department of Biochemistry, The national research centre for genetic engineering and biotechnology, Tehran 14155-6343, Iran. tafreshi@nrcgeb.ac.ir

Experimental allergic encephalomyelitis (EAE), a demyelinating disease induced in the animals parallels multiple sclerosis in human in several aspects, provides a useful model to investigate multiple sclerosis.

In this study, we have therefore used this model to study functions of nerve growth factor (NGF) in EAE. NGF with considerable effects on neuron survival, proliferation and differentiation of the nervous system, is also known to act on cells of the immune system. Simultaneous upregulation of proinflammatory cytokines and increased level of NGF points at possible effects of the nerve growth factor in autoimmune diseases. To investigate roles of NGF in experimental allergic encephalomyelitis in vivo, we therefore decided to apply it intracerebroventricularly at a dose of 0.20 mg/mice prior to the induction of EAE.

Our clinical observations showed that in the EAE induced animals who received NGF, severity of the disease was reduced significantly compared to that in saline treated EAE mice. Also neuropathological investigation of spinal cords revealed that in contrast to saline treated EAE mice, no signs of cell death, infiltration and demyelination can be seen in NGF treated EAE mice, suggesting that NGF may have clinical implications in multiple sclerosis.

PMID: 17237570 [PubMed - indexed for MEDLINE]

1: Clin Immunol. 2006 Jan;118(1):77-82. Epub 2005 Nov 7.

Neurotrophic factors in relapsing remitting and secondary progressive multiple sclerosis patients during interferon beta therapy.

Caggiula M, Batocchi AP, Frisullo G, Angelucci F, Patanella AK, Sancricca C, Nociti V, Tonali PA, Mirabella M.

Institute of Neurology, Catholic University, Largo Gemelli 8, 00168 Rome, Italy.

Although interferon (IFN) beta is a widely used disease-modifying therapy in multiple sclerosis (MS), the mechanisms responsible for its effects are not fully understood. Some studies demonstrated that IFNbeta induces nerve growth factor (NGF) secretion by astrocytes and by brain endothelial cells.

In this study, we determined the production of various neurotrophins (brain-derived neurotrophic factor, BDNF; NGF; glial cell line-derived neurotrophic factor; neurotrophin 3; neurotrophin 4) by peripheral blood mononuclear cells (PBMCs) in relapsing-remitting (RR) and secondary progressive (SP) MS patients during IFNbeta treatment.

There were no main variations in neurotrophin production either among all MS patients globally considered or in the group of SPMS subjects.

Instead, in the group of RRMS patients who did not present clinical exacerbation of disease up to the end of the study, we found a significant increase in BDNF production as from 6 months after starting therapy.

PMID: 16275091 [PubMed - indexed for MEDLINE]

Sorry folks the SALE is OVER!!! The CHEATERS ruined the sale!

You must now pay FULL PRICE for my "Brain Tonic".

Braindead

p.s I have heard that some folks have read the list of my ingredients and are getting them the from much, much cheaper sources. This is CHEATING--- shame on you!!!

Huh??? It's not nice to play with Mother's Nature's Brain!!!

tocotrienols = neuroprotection

--------------------------------------------------------------------------------

1: J Neurochem. 2006 Sep;98(5):1474-86.

Characterization of the potent neuroprotective properties of the natural vitamin
E alpha-tocotrienol.

Khanna S, Roy S, Parinandi NL, Maurer M, Sen CK.

Laboratory of Molecular Medicine, Department of Surgery, Davis Heart and Lung
Research Institute, The Ohio State University Medical Center, Colombus, Ohio
43210, USA.

The natural vitamin E tocotrienols possess properties not shared by tocopherols.
Nanomolar alpha-tocotrienol, not alpha-tocopherol, is potently neuroprotective.
On a concentration basis, this finding represents the most potent of all
biological functions exhibited by any natural vitamin E molecule. We sought to
dissect the antioxidant-independent and -dependent neuroprotective properties of
alpha-tocotrienol by using two different triggers of neurotoxicity, homocysteic
acid (HCA) and linoleic acid. Both HCA and linoleic acid caused neurotoxicity
with comparable features, such as increased ratio of oxidized to reduced
glutathione GSSG/GSH, raised intracellular calcium concentration and compromised
mitochondrial membrane potential. Mechanisms underlying HCA-induced
neurodegeneration were comparable to those in the path implicated in
glutamate-induced neurotoxicity. Inducible activation of c-Src and
12-lipoxygenase (12-Lox) represented early events in that pathway.
Overexpression of active c-Src or 12-Lox sensitized cells to HCA-induced death.
Nanomolar alpha-tocotrienol was protective. Knock-down of c-Src or 12-Lox
attenuated HCA-induced neurotoxicity. Oxidative stress represented a late event
in HCA-induced death. The observation that micromolar, but not nanomolar,
alpha-tocotrienol functions as an antioxidant was verified in a model involving
linoleic acid-induced oxidative stress and cell death. Oral supplementation of
alpha-tocotrienol to humans results in a peak plasma concentration of 3 microm.
Thus, oral alpha-tocotrienol may be neuroprotective by antioxidant-independent
as well as antioxidant-dependent mechanisms.

PMID: 16923160 [PubMed - indexed for MEDLINE]

1: Ann N Y Acad Sci. 2004 Dec;1031:127-42.

Tocotrienol: the natural vitamin E to defend the nervous system?

Sen CK, Khanna S, Roy S.

Davis Heart & Lung Research Institute, 473 West 12th Avenue, The Ohio State
University Medical Center, Columbus, Ohio 43210, USA. sen-1@medctr.osu.edu

Vitamin E is essential for normal neurological function. It is the major
lipid-soluble, chain-breaking antioxidant in the body, protecting the integrity
of membranes by inhibiting lipid peroxidation. Mostly on the basis of symptoms
of primary vitamin E deficiency, it has been demonstrated that vitamin E has a
central role in maintaining neurological structure and function. Orally
supplemented vitamin E reaches the cerebrospinal fluid and brain. Vitamin E is a
generic term for all tocopherols and their derivatives having the biological
activity of RRR-alpha-tocopherol, the naturally occurring stereoisomer compounds
with vitamin E activity. In nature, eight substances have been found to have
vitamin E activity: alpha-, beta-, gamma- and delta-tocopherol; and alpha-,
beta-, gamma- and delta-tocotrienol. Often, the term vitamin E is synonymously
used with alpha-tocopherol. Tocotrienols, formerly known as zeta, , or
eta-tocopherols, are similar to tocopherols except that they have an isoprenoid
tail with three unsaturation points instead of a saturated phytyl tail. Although
tocopherols are predominantly found in corn, soybean, and olive oils,
tocotrienols are particularly rich in palm, rice bran, and barley oils.

Tocotrienols possess powerful antioxidant, anticancer, and cholesterol-lowering
properties. Recently, we have observed that alpha-tocotrienol is multi-fold more
potent than alpha-tocopherol in protecting HT4 and primary neuronal cells
against toxicity induced by glutamate as well as by a number of other toxins. At
nanomolar concentration, tocotrienol, but not tocopherol, completely protected
neurons by an antioxidant-independent mechanism. Our current work identifies two
major targets of tocotrienol in the neuron: c-Src kinase and 12-lipoxygenase.
Dietary supplementation studies have established that tocotrienol, fed orally,
does reach the brain. The current findings point towards tocotrienol as a potent
neuroprotective form of natural vitamin E.

PMID: 15753140 [PubMed - indexed for MEDLINE]


1: Neuropharmacology. 2004 Nov;47(6):904-15.

Alpha-tocotrienol provides the most potent neuroprotection among vitamin E
analogs on cultured striatal neurons.

Osakada F, Hashino A, Kume T, Katsuki H, Kaneko S, Akaike A.

Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Kyoto
University, 46-29 Yoshida-shimoadachi-cho, Sakyo-ku, Kyoto 606-8501, Japan.

Oxidative stress and apoptosis play pivotal roles in the pathogenesis of
neurodegenerative diseases. We investigated the effects of vitamin E analogs on
oxidative stress and apoptosis using primary neuronal cultures of rat striatum.
A tocotrienol-rich fraction of edible oil derived from palm oil (Tocomin 50%),
which contains alpha-tocopherol, and alpha-, gamma- and delta-tocotrienols,
significantly inhibited hydrogen peroxide (H2O2)-induced neuronal death. Each of
the tocotrienols, purified from Tocomin 50% by high-performance liquid
chromatography, significantly attenuated H2O2-induced neurotoxicity, whereas
alpha-tocopherol did not. alpha-, gamma- and delta-Tocotrienols also provided
significant protection against the cytotoxicity of a superoxide donor, paraquat,
and nitric oxide donors, S-nitrosocysteine and 3-morpholinosydnonimine.
Moreover, tocotrienols blocked oxidative stress-mediated cell death with
apoptotic DNA fragmentation caused by an inhibitor of glutathione synthesis,
L-buthionine-[S,R]-sulfoximine. In addition, alpha-tocotrienol, but not gamma-
or delta-tocotrienol, prevented oxidative stress-independent apoptotic cell
death, DNA cleavage and nuclear morphological changes induced by a non-specific
protein kinase inhibitor, staurosporine. These findings suggest that
alpha-tocotrienol can exert anti-apoptotic neuroprotective action independently
of its antioxidant property. Among the vitamin E analogs examined,
alpha-tocotrienol exhibited the most potent neuroprotective actions in rat
striatal cultures.

PMID: 15527824 [PubMed - indexed for MEDLINE]