Reply #46: Well, if memory serves.... from the book The Brain Wellness Plan...

[HysteryDiagnosis]

persons who are susceptible to Parkinson's disease, (PD from now on) posess a gene that produces a weakened form of superoxide-dismutase, an enzyme I believe, that is responsible for mopping up stale neurotransmitters and possibly dealing with pesticides.... let me see.... yupper... we have a winner. This is not the only paper btw... go to the top of the page linked and enter your own search terms, I entered Parkinson's SOD to get this page up...

Mind you, The Brain Wellness Plan was published yeeeeeers ago. Now you see at the NIH a paper showing the veracity of the claims made therein. SOD, Coenzyme Q10 and a high quality form of vitamin E that contains alpha tocopherol and mixed tocopherols are all available at quality health food (Nutrition Science) stores just about everywhere.

If price is paramount, may I suggest www.vitaminshoppe.com

On EDIT: You certainly should acquaint yourself with the book Excitotoxins, the Taste That Kills" by Russell Blaylock board certified neurologist, and put down that diet soda if you have one...

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15193280
1: Cell Biol Int. 2004;28(5):373-80. Related Articles, Links

Protection against MPP+ neurotoxicity in cerebellar granule cells by antioxidants.

Gonzalez-Polo RA, Soler G, Rodriguezmartin A, Moran JM, Fuentes JM.

Departamento de Bioquimica y Biologia Molecular y Genetica, Facultad de Veterinaria, Universidad de Extremadura, Caceres, Spain.

The neuropathology associated with Parkinson's disease (PD) is thought to involve excessive production of free radicals, dopamine autoxidation, defects in glutathione peroxidase expression, attenuated levels of reduced glutathione, altered calcium homeostasis, excitotoxicity and genetic defects in mitochondrial complex I activity. While the neurotoxic mechanisms are vastly different for excitotoxins and 1-methyl-4-phenylpyridinium ion (MPP(+)), both are thought to involve free radical production, compromised mitochondrial activity and excessive lipid peroxidation. We show here that the levels of reactive oxygen species (ROS) and reactive nitrogen species (RNS) increased significantly after treatment of cultured cerebellar granule cells (CGCs) with 50 microM MPP(+).

Co-treatment with antioxidants such as ascorbate (ASC), catalase, alpha-tocopherol (alpha-TOH), coenzyme Q(10) (CoQ(10)) or superoxide dismutase (SOD) rescued the cells from MPP(+)-induced death. MPP(+)-induced cell death was also abolished by co-treatment with nitric oxide synthase (NOS) inhibitors such as 7-nitroindazole (7-NI), 2-ethyl-2-thiopseudourea hydrobromide (EPTU) or S-methylisothiourea sulphate (MPTU). We also tested the protective effects of an iron chelator (deferoxamine mesylate, DFx) and a peroxynitrite scavenger (FeTTPS) and the results lend further support to the view that the free radical cytotoxicity plays an essential role in MPP(+)-induced death in primary cultures of CGC.

PMID: 15193280