Journal of Neuroinflammation - Latest Comments

Questioning Caffeine/Alzheimer's Connection

Jeana Thomas — 2010-09-24T16:00:35Z

I simply have this question: How do we then explain the rampant Alzheimer's and other BBB diseases in the U.S. which is so universally addicted to caffeine?

geographic tongue relevant to brain autoimmunity?

Kelly Greenberg — 2009-04-14T14:23:28Z

I'm just a mom of an autistic three year old doing some late night reading and read your article. Every time my son regresses, he gets geographic tongue, which is also an autoimmune respose. I haven't read anything about a correlation, I guess that's why I'm mentioning it. Maybe someone will research this. I am sure they are connected in my son's case.

COX-2 inhibition by parecoxib and ischemic brain injury

Eduardo Candelario-Jalil — 2007-01-24T19:29:15Z

It is widely accepted that neuroinflammation is one of the mechanisms known to participate in the evolution of ischemic brain injury. Inhibition of the inducible isoform of cyclooxygenase (COX-2) has been shown to be neuroprotective in several models of brain damage including ischemic stroke. The article by Kelsen et al. provides additional information on the effects of parecoxib (the only COX-2 inhibitor clinically approved for intravenous administration) in an in vivo model of cerebral ischemia in rats. This is the first study to document the beneficial effects of a COX-2 inhibitor using the MRI technology. Interestingly, parecoxib treatment reduced ADC abnormalities one week after ischemia, which indicates, for the first time, the involvement of COX-2 in edema formation following ischemic stroke. Methods are sound and very well described. This study provides an interesting insight into the protective effect of parecoxib, and this report is a good example of how pre-clinical studies should be performed, in order to evaluate the neuroprotective efficacy of new drugs for the treatment of cerebral ischemia.

Oxidative - Redox stress by Beta amyloid may also be true for islet amyloid within pancreatic islets of those patients with metabolic syndrome and type 2 diabetes mellitus.

Melvin Hayden — 2004-11-16T19:30:31Z

Congratulations on an excellent study and the important findings regarding the effect of beta amyloid on lipoprotein oxidation.

We feel the same effect of islet amyloid might be occuring within the islets of the pancreata of patients with metabolic syndrome and type 2 diabetes mellitus. Islet amyloid and beta amyloid share many similar properties (including the polymerization and aggregation induced by free radical polymerization) and it is exciting that the translation of your findings to the islet in regards to hyperamylinemia and islet amyloid within the pancreas may possibly explain the delay in the development of overt type 2 diabetes mellitus with the use of pravastatin in the West of Scotland studies.

Hayden MR, Tyagi SC. Islet Redox Stress: The Manifold Toxicities of Insulin Resistance, Metabolic Syndrome and Amylin Derived Islet Amyloid in Type 2 Diabetes Mellitus. JOP. J Pancreas (Online) 2002; 3(4):86-108

Nicolls MR, D'Antonio JM, Hutton JC, Gill RG, Czwornog JL, Duncan MW. Proteomics as a tool for discovery: proteins implicated in Alzheimer's disease are highly expressed in normal pancreatic islets. J Proteome Res 2003; 2(2):199-205

Keep up the exciting work in this field and again kudos for this great and exciting paper.

Sincerely,

M.R. Hayden, M.D.