The blood brain barrier is the divide between inflammation (white blood cells etc) and neuroinflammation (glial cells). It is difficult to even see what is going on behind that wall, not to mention getting drugs past it as well. Scratching around PubMed did turn up a promise or two for those so inclined-

"Ethanol Extract of Magnolia officinalis Prevents Lipopolysaccharide-Induced Memory Deficiency via Its Antineuroinflammatory and Antiamyloidogenic Effects."

"Paeoniflorin attenuates neuroinflammation and dopaminergic neurodegeneration in the MPTP model of Parkinson's disease by activation of adenosine A1 receptor."http://www.ncbi.nlm.nih.gov/pubmed/16582933

"Epigallocatechin-3-gallate prevents systemic inflammation-induced memory deficiency and amyloidogenesis via its anti-neuroinflammatory properties."

The first is the tree, the second the peony flower if I remember correctly, and the third is green tea. All are commonly found at your health food store.

Here is an abstract that I just now found that sums it up nicely-


1. Curr Pharm Des. 2007;13(18):1925-8.

Inflammation in Parkinson's diseases and other neurodegenerative diseases: cause
and therapeutic implications.

Wilms H, Zecca L, Rosenstiel P, Sievers J, Deuschl G, Lucius R.

Department of Neurology, Christian-Albrechts-Universität Kiel, Germany.
h.wilms@neurologie.uni-kiel.de

Agents suppressing microglial activation are attracting attention as candidate
drugs for neuroprotection in Parkinson s disease (PD): While different mechanisms
including environmental toxins and genetic factors initiate neuronal damage in
the substantia nigra and striatum in PD, there is unequivocal evidence that
activation of neuroinflammatory cells aggravates this neurodegenerative process.
It was shown that following an acute exposure to the neurotoxin
1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and other toxins the
degenerative process continues for years in absence of the toxin. Reactive
microglia has been observed in the substantia nigra of patients with PD,
indicating that this inflammatory process might aggravate neurodegeneration. By
releasing various kinds of noxious factors such as cytokines or proinflammatory
molecules microglia may damage CNS cells. The stimuli triggering microgliosis in
Parkinsonian syndromes are unknown so far: However, analysis of neuronal loss in
PD patients shows that it is not uniform but that neurons containing neuromelanin
(NM) are predominantly involved. We hypothesized that extraneuronal melanin might
trigger microgliosis, microglial chemotaxis and microglial activation in PD with
subsequent release of neurotoxic mediators. The addition of human NM to
microglial cell cultures induced positive chemotactic effects, activated the
pro-inflammatory transcription factor nuclear factor kappa B (NF-kappaB) via
phosphorylation and degradation of the inhibitor protein kappaB (IkappaB), and
led to an upregulation of TNF-alpha, IL-6 and NO. These findings demonstrate a
crucial role of NM in the pathogenesis of Parkinson's disease by augmentation of
microglial activation, leading to a vicious cycle of neuronal death, exposure of
additional neuromelanin and chronification of inflammation. Antiinflammatory
drugs may be one of the new approaches in the treatment of PD.

PMID: 17584117 [PubMed - indexed for MEDLINE]

And finally, there was a brief mention of eliminating certain foods from one's diet. For me, at least, wheat is a killer. A single slice of bread will cost me the better part of a week of my life as I struggle back to where I was. My theory is that the gliadin in the wheat magnifies the neuroinflammatory reaction.

Thanks, Neil
I was surprised and disappointed by the paucity of data.
Jean

Any new contact with the Helen Foundation. I see that they are still around after a number of years, and it takes patients to keep the doors open.