The Relation of Oxidative Stress and Hyperexcitation to Neurological Disease

Abstract

The expression of a considerable range of neurological diseases is thought to involve two pathological states, namely, the production of excessive amounts of reactive oxygen species and neuronal hyperactivity. These events may represent an outcome of general vulnerable features of nervous tissue. Since they are associated with many unrelated diseases, the phenomena may be considered the final common pathways of a range of metabolic defects. Superimposed on these general signs of cellular impairment are the more specific features of each disorder. This review describes some of the evidence for the presence of hyperactivity and oxidative stress in various neurological disorders. Mechanisms whereby the states may interact and modulate each other are discussed. The manner in which such understanding has implications for the development of novel therapeutic approaches is also described.

Effect of an NMDA receptor antagonist and a ganglioside GM1 derivative upon ethanol-induced modification of parameters of oxidative stress in several brain regions

“…Such protective effects may have been related to the attenuation of glutamate-induced elevations of intracellular calcium. While excitotoxicity and oxidative stress are separate phenomena, there is a suspected but not clearly defined relation between these potentially harmful expressions of cell abnormality [3]. Both are undoubtedly relevant to the toxicity of ethanol and the report of Hoffman et al [23] shows that these features are closely related.…”

Neuroprotective Effect of Quercetin Encapsulated Liposomes: A Novel Therapeutic Strategy against Alzheimer's Disease

“…Various degrees of cognitive impairment were reported to be associated with cholinergic neuronal loss and dysfunction especially in AD (Bondy, 1995). A cholinergic function was previously reported to be required for short-term memory process and the cholinergic dysfunction also played a crucial role for short term memory deficit in AD (Galizia, 1984).…”

Altered Ca2+Signaling and Mitochondrial Deficiencies in Hippocampal Neurons of Trisomy 16 Mice: A Model of Down’s Syndrome

“…Furthermore, overexpression of Cu / Z n-SOD (Groner et al, 1994) and ␤APP via the product ␤AP can cause an increased production of ROS (Behl et al, 1994). Elevated ROS concentration is known to cause mitochondrial damage (Beal et al, 1993;Dykens, 1994;Bolaños et al, 1995Bolaños et al, , 1997) and disturb C a 2ϩ homeostasis (Richter and Kass, 1991;Gunter et al, 1994;Mattson, 1994;Bondy, 1995;Mattson et al, 1995;White and Reynolds, 1996). Further studies on the Ts16 mouse model are needed to determine whether the primary defect is linked to C a 2ϩ homeostasis or mitochondrial ROS production.…”