Cell Death Signaling

Cold Spring Harbor Perspectives in Biology, Journal Year: 2015, Volume and Issue: 7(12), P. a006080 - a006080

Published: Dec. 1, 2015

Douglas R. Green and Fabien Llambi Department of Immunology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105 Correspondence: douglas.green{at}stjude.org

Language: Английский

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Calcium, ischemia and excitotoxicity

Cell Calcium, Journal Year: 2010, Volume and Issue: 47(2), P. 122 - 129

Published: Feb. 1, 2010

Language: Английский

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Calcium signaling and neurodegenerative diseases

Trends in Molecular Medicine, Journal Year: 2009, Volume and Issue: 15(3), P. 89 - 100

Published: Feb. 22, 2009

Language: Английский

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The calpain system and cancer

Nature reviews. Cancer, Journal Year: 2011, Volume and Issue: 11(5), P. 364 - 374

Published: April 21, 2011

Language: Английский

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Mitochondrial Dysfunction and Myocardial Ischemia-Reperfusion: Implications for Novel Therapies

The Annual Review of Pharmacology and Toxicology, Journal Year: 2016, Volume and Issue: 57(1), P. 535 - 565

Published: Nov. 18, 2016

Mitochondria have emerged as key participants in and regulators of myocardial injury during ischemia reperfusion. This review examines the sites damage to cardiac mitochondria focuses on impact these defects. The concept that mitochondrial leads reperfusion is addressed. mechanisms translate ischemic into cellular damage, both early reperfusion, are examined. Next, we discuss strategies modulate counteract mitochondrial-driven injury. new not merely stochastic oxidative calcium-mediated but they activate responses remodeling reactions balance between cell death recovery reviewed, therapeutic implications this discussed.

Language: Английский

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The dysregulation of intracellular calcium in Alzheimer disease

Cell Calcium, Journal Year: 2010, Volume and Issue: 47(2), P. 183 - 189

Published: Jan. 19, 2010

Language: Английский

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Comprehensive review of mechanisms of pathogenesis involved in Alzheimer’s disease and potential therapeutic strategies

Progress in Neurobiology, Journal Year: 2018, Volume and Issue: 174, P. 53 - 89

Published: Dec. 30, 2018

Language: Английский

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Glutamate system, amyloid β peptides and tau protein: functional interrelationships and relevance to Alzheimer disease pathology

Journal of Psychiatry and Neuroscience, Journal Year: 2012, Volume and Issue: 38(1), P. 6 - 23

Published: Dec. 19, 2012

Alzheimer disease is the most prevalent form of dementia globally and characterized premortem by a gradual memory loss deterioration higher cognitive functions postmortem neuritic plaques containing amyloid ß peptide neurofibrillary tangles phospho-tau protein. Glutamate abundant neurotransmitter in brain essential to formation through processes such as long-term potentiation so might be pivotal progression. This review discusses how glutamatergic system impaired interactions glutamate influence synaptic function, tau phosphorylation neurodegeneration. Interestingly, not only influences production, but also can alter levels at synapse, indicating that small changes concentrations both molecules could Finally, we describe receptor antagonist, memantine, has been used treatment individuals with discuss its effectiveness.

Language: Английский

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α-Lipoic acid improves abnormal behavior by mitigation of oxidative stress, inflammation, ferroptosis, and tauopathy in P301S Tau transgenic mice

Redox Biology, Journal Year: 2017, Volume and Issue: 14, P. 535 - 548

Published: Nov. 7, 2017

Alzheimer's disease (AD) is the most common neurodegenerative and characterized by neurofibrillary tangles (NFTs) composed of Tau protein. α-Lipoic acid (LA) has been found to stabilize cognitive function AD patients, animal study findings have confirmed its anti-amyloidogenic properties. However, underlying mechanisms remain unclear, especially with respect ability LA control pathology neuronal damage. Here, we that supplementation effectively inhibited hyperphosphorylation at several AD-related sites, accompanied reduced decline in P301S transgenic mice. Furthermore, not only activity calpain1, which associated tauopathy development neurodegeneration via modulating kinases, but also significantly decreased calcium content brain tissue LA-treated Next, screened for various modes neural cell death We caspase-dependent apoptosis was potently inhibited, whereas autophagy did show significant changes after supplementation. Interestingly, Tau-induced iron overload, lipid peroxidation, inflammation, are involved ferroptosis, were blocked administration. These results provide compelling evidence plays a role inhibiting loss, including through pathways, suggesting may be potential therapy tauopathies.

Language: Английский

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Molecular mechanisms of cognitive dysfunction following traumatic brain injury

Frontiers in Aging Neuroscience, Journal Year: 2013, Volume and Issue: 5

Published: Jan. 1, 2013

Traumatic brain injury (TBI) results in significant disability due to cognitive deficits particularly attention, learning and memory higher-order executive functions. The role of TBI chronic neurodegeneration the development neurodegenerative diseases including Alzheimer's disease (AD), Parkinson's (PD), Amyotrophic Lateral Sclerosis (ALS) most recently traumatic encephalopathy (CTE) is particular importance. However, despite effort very few therapeutic options exist prevent or reverse impairment following TBI. In this review we present experimental evidence known secondary mechanisms which contribute neuronal cell loss, axonal synaptic dysfunction hence both acutely chronically focus on linking two forms dementia: AD CTE. We provide potential molecular involved modulating Aβ Tau these pathology. Additionally propose a mechanism by generated as direct result capable exacerbating thereby establishing neurotoxic cascade that leads neurodegeneration.

Language: Английский

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