Finn
That's more fascinating info:
So, if Matzinger is right, the immune response would be a reaction to abnormal cell death, not the primary reason for nerve damage.
Actually, some of the info on BDNF and MS seems to be consistent with Matzinger’s theory. There’s research indicating relapses elicit a “protective response”, i.e., BDNF levels increase during relapses.
Brain-derived neurotrophic factor in patients with multiple sclerosis
On the basis of recent experimental findings, a neuroprotective effect of BDNF produced by inflammatory cells can be hypothesized during relapses in MS. This can favor remyelination. The reduced production of BDNF by PBMCs of patients with SP MS can contribute to the progression of demyelinating disease and axonal loss in this form.
Regarding the
association between low BDNF levels and disability progression the researchers found:
Significantly lower BDNF values were found in unstimulated and stimulated PBMC supernatants of patients with SP MS compared to control subjects. This reduction was greater in patients with a 1-point increase in the EDSS score in the last 6 months compared with that in patients without a progression of the disability score. Reduction in the levels of BDNF was also confirmed in the CSF of SP MS patients compared with R-R MS patients assessed during a stable phase of the disease and control subjects.
Now, to your question:
So far I have come across two things that may be able to increase BDNF: exercise and some antidepressants. Do you happen to have information on other substances that might be able to do it?
Besides exercise and some antidepressants, voila,
estrogen and progesterone might also be able to increase BDNF (actually, they may have a role in regulating or modulating BDNF levels).
Influence of endogenous and exogenous sex hormones on plasma brain-derived neurotrophic factor
The aim of this study is to assess plasma BDNF variations according to hormonal status
BDNF was positively correlated with E(2) and progesterone and negatively correlated with menopausal age. HRT restored BDNF levels to those present in fertile women during the follicular phase. CONCLUSIONS: Plasma BDNF levels are influenced by hormonal status. Modifications in BDNF circulating levels during the menstrual cycle suggest a potential role for gonadal sex hormones (E(2) and progesterone) in regulating neurotrophin expression
And, specific to progesterone, there’s this recent
research focused on the brain (mice).
In addition, at a concentration and duration of treatment consistent with our neuroprotection data, progesterone also increased the expression of brain-derived neurotrophic factor (BDNF), at the level of both protein and mRNA.
So, and I think I asked it earlier in this thread, I think it’s very legitimate to once again ask: Is the decline in hormone levels with age a factor that might just contribute to disease progression?
There’s
research linking low estrogen and progesterone levels to low levels of BDNF and there’s
research linking low BDNF levels to disease progression. Personally, I think it’s becoming harder and harder to totally ignore a possible connection between hormone levels and disease progression. Especially in light of the recent research linking EDSS scores with age. Just my very biased opinion, again.
And, for people with an interest in diet and supplements, there are some other things associated with BDNF levels. Saturated fat apparently lowers BDNF levels (hello Dr. Swank).
Vitamin E can help offset that.
A diet high in saturated fat (HF) decreases levels of brain-derived neurotrophic factor (BDNF),
Supplementation of the HF diet with vitamin E dramatically reduced oxidative damage, normalized levels of BDNF, synapsin I and cyclic AMP-response element-binding protein (CREB), caused by the consumption of the HF diet.
Curcumin might also “normalize” BDNF levels.
Supplementation of curcumin in the diet dramatically reduced oxidative damage and normalized levels of BDNF, synapsin I, and CREB that had been altered after TBI.
Omega –3 fatty acids (DHA) may also help “normalize” BDNF levels.
Supplementation of omega-3 fatty acids in the diet counteracted all of the studied effects of FPI, that is, normalized levels of BDNF.
And, Lynda Carol, check this out,
low BDNF levels are associated with “insulin resistance”. Per this
abstract It is known that a high sugar, high fat diet leads to reduced brain expression of brain-derived neurotrophic factor (BDNF) which is responsible for maintaining the outgrowth of dendrites. Low brain BDNF levels also lead to insulin resistance.
Finally,
Copaxone also appears to impact BDNF levels. And, that’s it for the moment on BDNF.
Finn
Well, this is a consensus autoimmune board now, and I try not to corrupt the spirit by posting more here
But if I find something really interesting, I promise I'll make an exception and share it.
I agree with you that it’s a consensus autoiummune board at the moment. However, unlike you I occasionally have to corrupt the spirit, or, so I'm sure it seems to some. But, I continue to think there’s value in different points of view, so I’m glad to know if you find something really interesting that you’ll post it.
There was actually some recent research that doesn't seem to particularly bolster the MS is “auto-immune” perspective.
Cerebrospinal fluid oligoclonal bands and progression of disability in multiple sclerosis Antibody-mediated inflammation is believed to contribute to tissue injury in multiple sclerosis (MS).
There were no differences in presence or number of CSF OCB between patients with significant worsening of disability and stable patients. There were no differences in presence or number of CSF OCB between patients with stable relapsing-remitting MS and patients developing secondary progression during follow-up. The presence or number of CSF OCB does not seem to influence early disease progression in MS.
The beat and the debate will continue I guess--hopefully even occasionally on this board.
Take care all
Sharon
The number of transected axons per cubic millimeter of tissue averaged 11,236 in active lesions, 3138 at the hypocellular edges of chronic active lesions, 875 in the hypocellular centers of chronic active lesions, and less than 1 in normal-appearing white matter from the control brains. 