Aluminum excytotoxicity and neuroautotoimmunity: the role of the brain expression of CD32+ (FcγRIIa), ICAM-1+ and CD3ξ in aging.

In the central nervous system (CNS) microglia are crucial for the defense of the brain against invading microorganisms, formation of tumors, and damage following trauma. However, uncontrolled activation of these cells may have deleterious outcomes through activation of Fcγ and the complement 3 receptors and the induction of an adaptive immune reaction. Proteins contributing to this reaction are the intercellular adhesion molecule-1 (ICAM-1) and CD3 molecules, among others. Both can be expressed on the glia cells before cytokine release and may facilitate an autoimmune inflammatory reaction in the brain. Round microglial cells among the pyramidal cells of the hippocampus with increased expression of CD32+ (FcγIIa) and near the site of injection of aluminum were detected immunohistochemically and indicate microglial activation at the site of aluminum injury. ICAM-1+ immunoreactivity significantly increased in the hippocampus and in the choroids plexus, indicating increased inflammation in the brain as well as increased CD3ξ+ expression in the hippocampus and non-MHC-restricted T cytotoxicity after aluminum injection. The pattern of expression of CD32+ (FcγIIa receptor) near the site of aluminum injection indicates that microglia may play a phagocytic role at the site of aluminum-induced excitotoxicity in the brain. Significant expression of ICAM-1+ and CD3ξ+ immunoreactive cells with the clusters of ICAM-1+ in the choroid plexus suggests a consequently neurotoxic autoimmune reaction induced by microglial hyperactivation in the injured brain.

From the global to the local: possible pathways for the transduction of Indo-Sino-Tibetan cognitive-behavioral practices into site-specific, tissue-regenerative effects.

While skepticism regarding the possibilities for a productive meeting (metaphorically or actual) between Western medicine and biology and older healing and health practices of traditional cultures may be prevalent, there are many theoretical points of meeting and much experimental data to suggest that cognitive-behavioral practices (C-Bp) of the latter may induce testable and reproducible phenomena for the former. Such modulation or modification of tissue regeneration by C-Bp presumably must work through systemic signaling of some kind. Several possible mechanisms for such signaling are recognized and will be reviewed here: humoral, neurological, cell trafficking, and bioelectromagnetic/energy mediated. Nonetheless, while cultures and techniques may be varied, human bodies are more alike than dissimilar. We indicate that great profit may be had for all participating cultures in establishing a common language, shared criteria for designing experiments and interpreting data, and cooperative goals for the promotion of tissue integrity and regeneration.

MAgnetic stimulation of the brain increase Na+, K+-ATPase activity decreased by injection of AlCl3 into nucleus basalis magnocellularis of rats.

This article reports here on the influence of the static magnetic fields (MFs), locally applied to the brain area, on Na, K-ATPase activity in the rat with lesioned nucleus basalis magnocellularis (NBM) by intracerebral injection of 5 microl, 1% AlCl3 into the nucleus. Two AKMA micromagnets (M) flux density of 60 miliTesla, 5 mm in diameter, were bilaterally implanted with "N" polarity facing down to the cranial bones in the vicinity of the pineal gland (PG), immediately after the lesioning of NBM, during the same operation procedure. Ten days after the lesions of NBM, Na, K-ATPase activity on the erythrocyte membranes in the peripheral blood, measured spectrophotometrically, was completely inhibited. Magnetic stimulation (60 mT) of the brain during the 10 days significantly increased Na, K-ATPase activity on the erythrocyte membranes of rats with lesioned NBM. This results suggests that altered by lesions Na, K-ATPase activity in an experimental model of Alzheimer's disease might be ameliorated by magnetic stimulation of the brain.