Neuronal damage

Early neuronal damage detected by immunohistochemistry has been confirmed by brain magnetic resonance spectroscopy (MRS) analysis of the neuronal marker N-acetylaspartate (NAA) (commonly expressed as an NAA/creatine ratio NAA/ Cr) in the acute and chronic phases of infection in SIV-infected macaques (Fuller et al. 2004 Greco et al. 2004 Lentz et al. 2005 Lentz et al. 2008 Williams et al. 2005). In a macaque model involving CD8h- T lymphocyte depletion along with SIV inoculation, Williams et al. (2005) demonstrated a reduction in NAA/Cr in the... 

Toggas SM, Masliah E, Mucke L (1996) Prevention of HIV-1 gpl20-induced neuronal damage in the central nervous system of transgenic mice by the NMDA receptor antagonist memantine. Brain Res 706 303-307... 

Tomassini N, Renaud F, Roy S, Loh HH (2004) Morphine inhibits Fc-mediated phagocytosis through mu and delta opioid receptors. J Neuroimmunol 147 131-133 Trillo-Pazos G, Kandanearatchi A, Eyeson J, King D, Vyakamam A, Everall IP (2004) Infection of stationary human brain aggregates with HIV-1 SF162 and IIIB results in transient neuronal damage and neurotoxicity. Neuropathol Appl Neurobiol 30 136-147... 

Barth A, Barth L, Newell DW. Combination therapy with mk-801 and alpha-phenyl-tert-butyl-nitrone enhances protection against ischemic neuronal damage in organotypic hippocampal slice cultures. Exp Neurol 1996 141 330-336. 

Tso and Lam suggested that astaxanthin could be useful for prevention and treatment of neuronal damage associated with age-related macular degeneration and may also be effective in treating ischemic reperfusion injury, Alzheimer s disease, Parkinson s disease, spinal cord injuries, and other types of central nervous system injuries. Astaxanthin was found to easily cross the blood-brain barrier and did not form crystals in the eye. 

The purported prophylactic use of Japanese herbal medicines to combat neuronal ageing has been related to their free-radical scavenging activity (Hiramatsu a al., 1992). Inhibition of the pro-inflammatory effects of cytokine interleukin-1 by recombinant endogenous interleukin-1 receptor antagonist in experimental rats is associated with alleviation of excitotoxic neuronal damage, an action which has also been related to the antiinflammatory effect of lipocortin 1 (Relton and Roth well, 1992). 

During ischaemia, NOS is activated by calcium influx or by cytokines like tumour necrosis factor (TNF) or by lipopolysaccharide (LPS) and NO is produced in excess. It has been proposed that the excitotoxic effect of glutamate, which contributes to ischaemia-induced neuronal damage, is mediated by increased production of NO via a chain of events that includes increases in intracellular calcium (via glutamate activation of NMDA receptors), calcium activation of NOS, production of NO and peroxynitrite, and induction of lipid peroxidation. In fact, N-nitro-L-atginine, a selective inhibitor of NOS, has been shown to prevent glutamate-induced neurotoxicity in cortical cell cultures (Dawson rf /., 1991). 

A series of dihydrodibenzoxepines, represented by AJ3941, was tested in animal models of global ischaemia and hypoxia, and found to be protective. AJ3941 is an inhibitor of lipid peroxidation (Kurakawa etal., 1991). A novel quinazoline fumarate (KB56666, was found to inhibit lipid peroxidation in rat brain homogenates and isolated mitochondria. In a rat focal stroke model, KE56666 prevented brain oedema and neuronal damage in the ischaemic zone (Hara etal., 1991). 

Inui K, Mitsumori K, Harada T, et al. 1993. Quantitative analysis of neuronal damage induced by tri-ortho-cresyl phosphate in Wistar rats. Fundam Appl Toxicol 20 111-119. 

The major clinical problem arising from IM injections is muscle or neuron damage, the injury normally resulting from faulty technique, rather than the medication. Most injectable products can be given intramuscularly, with a normal onset of action from 15... 

Histopathological findings in fatal cases of lead encephalopathy in children include cerebral edema, altered capillaries, and perivascular glial proliferation. Neuronal damage is variable and may be caused by anoxia (EPA 1986a). 

DeVito, M.J., Wagner, G.C. Methamphetamine-induced neuronal damage a possible role for free radicals. Neuropharmacology. 28 1145, 1989. 

Large numbers of generalized tonic-clonic (GTC) seizures (more than 100) and multiple episodes of status epilepticus may be associated with neuronal damage. In particular, continued exposure to glutamate may contribute to neuronal damage. 

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