This abstract was published yesterday on PubMed. It’s about a German study of “cerebral depletion in high-energy phosphates” in PSP. It’s challenging reading because many of the terms and concepts are new to me. One of the authors, Dr. Hoglinger, is one of the stars of PSP research. I will email him regarding the implications of this research (or perhaps Ed can?).
One implication *might* be that PSP patients could benefit from taking creatine. The NIH has been studying whether creatine provides a neuroprotective effect in Parkinson’s Disease. Creatine is used by body builders to build muscle.
Local group member Sam gave his partner Eva creatine on a daily basis. He had this to say a few years ago: “Supposedly 10 grams a day of creatine is helpful; that’s about a teaspoonful. We found that straight Creatine powder–no additives chemicals– dissolves poorly in liquid, and settles sludge-like at the bottom, so we stopped using it. But recently we started adding Maximum Crea-Gain (800/808-8800 or www.energienutrition.com) to the morning juice and it mixes well. It has a dab of artificial flavor, which I don’t like, but is better than other creatine blends which are loaded with dyes and flavor chemicals.” After Eva died, I asked Sam about use of creatine; he said: “Yes, I continued squeezing CoQ10 and mixing creatine with her food to the end, and would keep doing that. They were easy additives and possibly of benefit. No reason to stop them.”
That’s about all I know regarding creatine…. If anyone understands the abstract below, please share!
Journal of Cerebral Blood Flow & Metabolism. 2009 Feb 4. [Epub ahead of print]
In vivo evidence for cerebral depletion in high-energy phosphates in progressive supranuclear palsy.
Stamelou M, Pilatus U, Reuss A, Magerkurth J, Eggert KM, Knake S, Ruberg M, Schade-Brittinger C, Oertel WH, Höglinger GU.
Department of Neurology, Philipps University, Marburg, Germany.
Indirect evidence from laboratory studies suggests that mitochondrial energy metabolism is impaired in progressive supranuclear palsy (PSP), but brain energy metabolism has not yet been studied directly in vivo in a comprehensive manner in patients.
We have used combined phosphorus and proton magnetic resonance spectroscopy to measure adenosine-triphosphate (ATP), adenosine-diphosphate (ADP), phosphorylated creatine, unphosphorylated creatine, inorganic phosphate and lactate in the basal ganglia and the frontal and occipital lobes of clinically probable patients (N=21; PSP stages II to III) and healthy controls (N=9).
In the basal ganglia, which are severely affected creatine in PSP patients, the concentrations of high-energy phosphates (=ATP+phosphorylated creatine) and inorganic phosphate, but not low-energy phosphates (=ADP+unphosphorylated creatine), were decreased. The decrease probably does not reflect neuronal death, as the neuronal marker N-acetylaspartate was not yet significantly reduced in the early-stage patients examined.
The frontal lobe, also prone to neurodegeneration in PSP, showed similar alterations, whereas the occipital lobe, typically unaffected, showed less pronounced alterations.
The levels of lactate, a product of anaerobic glycolysis, were elevated in 35% of the patients.
The observed changes in the levels of cerebral energy metabolites in PSP are consistent with a functionally relevant impairment of oxidative phosphorylation.
PubMed ID: 19190655 (see pubmed.gov for this abstract only)