Ketones inhibit mitochondrial production of reactive oxygen species production following glutamate excitotoxicity by increasing NADH oxidation
M Maalouf, PG Sullivan, L Davis, DY Kim, JM Rho - Neuroscience, 2007 - Elsevier
Dietary protocols that increase serum levels of ketones, such as calorie restriction and the
ketogenic diet, offer robust protection against a multitude of acute and chronic neurological …
ketogenic diet, offer robust protection against a multitude of acute and chronic neurological …
The ketogenic diet increases mitochondrial uncoupling protein levels and activity
PG Sullivan, NA Rippy, K Dorenbos… - Annals of …, 2004 - Wiley Online Library
Fatty acids are known to enhance mitochondrial uncoupling protein (UCP) activity. We asked
whether a high‐fat ketogenic diet (KD) increases UCP levels and activity in hippocampi of …
whether a high‐fat ketogenic diet (KD) increases UCP levels and activity in hippocampi of …
Modulation of mitochondrial function by endogenous Zn2+ pools
SL Sensi, D Ton-That, PG Sullivan… - Proceedings of the …, 2003 - National Acad Sciences
Recent evidence suggests that intracellular Zn 2+ accumulation contributes to the neuronal
injury that occurs in epilepsy or ischemia in certain brain regions, including hippocampus, …
injury that occurs in epilepsy or ischemia in certain brain regions, including hippocampus, …
Dietary supplement creatine protects against traumatic brain injury
PG Sullivan, JD Geiger, MP Mattson… - Annals of …, 2000 - Wiley Online Library
Creatine, one of the most common food supplements used by individuals at almost every
level of athleticism, promote gains in performance, strength, and fat‐free mass. Recent …
level of athleticism, promote gains in performance, strength, and fat‐free mass. Recent …
Cyclosporin A attenuates acute mitochondrial dysfunction following traumatic brain injury
PG Sullivan, MB Thompson, SW Scheff - Experimental neurology, 1999 - Elsevier
Experimental traumatic brain injury (TBI) results in a rapid and significant necrosis of cortical
tissue at the site of injury. In the ensuring hours and days, secondary injury exacerbates the …
tissue at the site of injury. In the ensuring hours and days, secondary injury exacerbates the …
Time course of post-traumatic mitochondrial oxidative damage and dysfunction in a mouse model of focal traumatic brain injury: implications for neuroprotective …
IN Singh, PG Sullivan, Y Deng… - Journal of Cerebral …, 2006 - journals.sagepub.com
In the present study, we investigate the hypothesis that mitochondrial oxidative damage and
dysfunction precede the onset of neuronal loss after controlled cortical impact traumatic …
dysfunction precede the onset of neuronal loss after controlled cortical impact traumatic …
Inflammation induces mitochondrial dysfunction and dopaminergic neurodegeneration in the nigrostriatal system
…, HC Kim, WA Cass, PG Sullivan, G Bing - Journal of …, 2007 - Wiley Online Library
Evidence suggests that chronic inflammation, mitochondrial dysfunction, and oxidative
stress play significant and perhaps synergistic roles in Parkinson’s disease (PD), where the …
stress play significant and perhaps synergistic roles in Parkinson’s disease (PD), where the …
Increase in blood–brain barrier permeability, oxidative stress, and activated microglia in a rat model of blast‐induced traumatic brain injury
…, JR Pauly, RM McCarron, PG Sullivan - Journal of …, 2010 - Wiley Online Library
Traumatic brain injury (TBI) as a consequence of exposure to blast is increasingly prevalent
in military populations, with the underlying pathophysiological mechanisms mostly unknown. …
in military populations, with the underlying pathophysiological mechanisms mostly unknown. …
Spatial and temporal characteristics of neurodegeneration after controlled cortical impact in mice: more than a focal brain injury
ED Hall, PG Sullivan, TR Gibson, KM Pavel… - Journal of …, 2005 - liebertpub.com
The present study examined the neuropathology of the lateral controlled cortical impact (CCI)
traumatic brain injury (TBI) model in mice utilizing the de Olmos silver staining method that …
traumatic brain injury (TBI) model in mice utilizing the de Olmos silver staining method that …
[HTML][HTML] Zn2+ induces permeability transition pore opening and release of pro-apoptotic peptides from neuronal mitochondria
Rapid entry of Ca 2+ or Zn 2+ kills neurons. Mitochondria are major sites of Ca 2+ -dependent
toxicity. This study examines Zn 2+ -initiated mitochondrial cell death signaling. 10 nm Zn …
toxicity. This study examines Zn 2+ -initiated mitochondrial cell death signaling. 10 nm Zn …