Glutamate receptors, neurotoxicity and neurodegeneration

A Lau, M Tymianski - Pflügers Archiv-European Journal of Physiology, 2010 - Springer
Glutamate excitotoxicity is a hypothesis that states excessive glutamate causes neuronal
dysfunction and degeneration. As glutamate is a major excitatory neurotransmitter in the …

PARP-1 cleavage fragments: signatures of cell-death proteases in neurodegeneration

GV Chaitanya, JS Alexander, PP Babu - Cell communication and signaling, 2010 - Springer
The normal function of poly (ADP-ribose) polymerase-1 (PARP-1) is the routine repair of
DNA damage by adding poly (ADP ribose) polymers in response to a variety of cellular …

Inhibition of caspase 3 and caspase 9 mediated apoptosis: a multimodal therapeutic target in traumatic brain injury

A Unnisa, NH Greig, MA Kamal - Current neuropharmacology, 2023 - benthamdirect.com
Traumatic brain injury (TBI) is one of the significant causes of death and morbidity, and it is
hence a focus of translational research. Apoptosis plays an essential part in the …

Traumatic brain injury: can the consequences be stopped?

E Park, JD Bell, AJ Baker - Cmaj, 2008 - Can Med Assoc
Traumatic brain injury is a leading cause of morbidity and death in both industrialized and
develo** countries. To date, there is no targeted pharmacological treatment that effectively …

In vitro models of traumatic brain injury

B Morrison III, BS Elkin, JP Dollé… - Annual review of …, 2011 - annualreviews.org
In vitro models of traumatic brain injury (TBI) are hel** elucidate the pathobiological
mechanisms responsible for dysfunction and delayed cell death after mechanical stimulation …

Neurons respond directly to mechanical deformation with pannexin‐mediated ATP release and autostimulation of P2X7 receptors

J **a, JC Lim, W Lu, JM Beckel… - The Journal of …, 2012 - Wiley Online Library
Key points• Neurons can be damaged when tissues are stretched or swollen; while
astrocytes can contribute to this process, the mechanosensitive response from neurons is …

PARP-1 inhibition attenuates neuronal loss, microglia activation and neurological deficits after traumatic brain injury

BA Stoica, DJ Loane, Z Zhao, SV Kabadi… - Journal of …, 2014 - liebertpub.com
Traumatic brain injury (TBI) causes neuronal cell death as well as microglial activation and
related neurotoxicity that contribute to subsequent neurological dysfunction. Poly (ADP …

Saikosaponin-D reduces cisplatin-induced nephrotoxicity by repressing ROS-mediated activation of MAPK and NF-κB signalling pathways

X Ma, C Dang, H Kang, Z Dai, S Lin, H Guan… - International …, 2015 - Elsevier
The nephrotoxicity induced by cisplatin (DDP) severely limits the clinical efficacy of this
widely used anticancer agent. The observed nephrotoxicity may be the result of DDP …

Temporal relationship of peroxynitrite-induced oxidative damage, calpain-mediated cytoskeletal degradation and neurodegeneration after traumatic brain injury

Y Deng, BM Thompson, X Gao, ED Hall - Experimental neurology, 2007 - Elsevier
We assessed the temporal and spatial characteristics of PN-induced oxidative damage and
its relationship to calpain-mediated cytoskeletal degradation and neurodegeneration in a …

Cellular mechanisms of peroxynitrite-induced neuronal death

K Ramdial, MC Franco, AG Estevez - Brain research bulletin, 2017 - Elsevier
Peroxynitrite (ONOO−) is a strong biological oxidant formed by the diffusion-limited reaction
of nitric oxide (NO−) and superoxide anion (O 2 radical dot−). It has long been theorized that …