Oxidative stress, DNA damage, and the telomeric complex as therapeutic targets in acute neurodegeneration

Article ID	Journal	Published Year	Pages	File Type
10958100	Neurochemistry International	2013	12 Pages	PDF

Abstract

âº Oxidative stress is a major contributor to acute CNS injury and disease. âº A major consequence of excessive ROS/RNS production is DNA damage. âº Unrepaired DNA damage initiates signaling cascades for neuron death. âº The telomeric complex may modulate the pro-apoptotic response to DNA damage. âº DNA damage and telomerase remain strong candidates for therapy in CNS injury.

Keywords

APAF1 CCI SOD1 8-oxoG HHS POT1 SSB PROG OGG1 DNA-PKcs DSB 8-Nitroguanine NEIL1 TERC MDA PFT-α pifithrin-α Telomerase RNA component endonuclease VIII-like 1 EAE PARP-1 4-HNE 4-hydroxynonenal TRF APE 8-oxoguanine DNA glycosylase apurinic/apyrimidinic endonuclease ataxia-telangiectasia mutated PIKK xeroderma pigmentosum CNS injury DNA damage experimental allergic encephalomyelitis AIF amyotrophic lateral sclerosis checkpoint kinase ALS TERT Telomerase reverse transcriptase Telomere Telomerase Oxidative stress protection of telomeres 1 ATM BBB superoxide dismutase 1 double strand break single strand break Apoptotic protease-activating factor 1 apoptosis-inducing factor malondialdehyde Methylprednisolone Neuron death NAD nicotinamide adenine dinucleotide 8-hydroxyguanosine DNA-dependent protein kinase catalytic subunit Progesterone poly (ADP-ribose) polymerase-1 Chk controlled cortical impact Dyskeratosis congenita