TopicNeuroscience

mitochondrial dysfunction

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31Total items

29ePosters

2Seminars

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SeminarNeuroscience

Mechanisms Underlying the Persistence of Cancer-Related Fatigue

Elisabeth G. Vichaya

Baylor University

May 23, 2023

Cancer-related fatigue is a prominent and debilitating side effect of cancer and its treatment. It can develop prior to diagnosis, generally peaks during cancer treatment, and can persist long after treatment completion. Its mechanisms are multifactorial, and its expression is highly variable. Unfortunately, treatment options are limited. Our research uses syngeneic murine models of cancer and cisplatin-based chemotherapy to better understand these mechanisms. Our data indicate that both peripherally and centrally processes may contribute to the developmental of fatigue. These processes include metabolic alterations, mitochondrial dysfunction, pre-cachexia, and inflammation. However, our data has revealed that behavioral fatigue can persist even after the toxicity associated with cancer and its treatment recover. For example, running during cancer treatment attenuates kidney toxicity while also delaying recovery from fatigue-like behavior. Additionally, administration of anesthetics known to disrupt memory consolidation at the time treatment can promote recovery, and treatment-related cues can re-instate fatigue after recovery. Cancer-related fatigue can also promote habitual behavioral patterns, as observed using a devaluation task. We interpret this data to suggest that limit metabolic resources during cancer promote the utilization of habit-based behavioral strategies that serve to maintain fatigue behavior into survivorship. This line of work is exciting as it points us toward novel interventional targets for the treatment of persistent cancer-related fatigue.

SeminarNeuroscienceRecording

Redox and mitochondrial dysregulation in epilepsy

Manisha Patel

University of Colorado

Sep 21, 2022

Epileptic seizures render the brain uniquely dependent on energy producing pathways. Studies in our laboratory have been focused on the role of redox processes and mitochondria in the context of abnormal neuronal excitability associated with epilepsy. We have shown that that status epilepticus (SE) alters mitochondrial and cellular redox status, energetics and function and conversely, that reactive oxygen species and resultant dysfunction can lead to chronic epilepsy. Oxidative stress and neuroinflammatory pathways have considerable crosstalk and targeting redox processes has recently been shown to control neuroinflammation and excitability. Understanding the role of metabolic and redox processes can enable the development of novel therapeutics to control epilepsy and/or its comorbidities.

mitochondrial dysfunction

Latest

Mechanisms Underlying the Persistence of Cancer-Related Fatigue

Redox and mitochondrial dysregulation in epilepsy

INFLAMMATION‑LINKED MITOCHONDRIAL DYSFUNCTION IN PTSD SUSCEPTIBILITY

ABLATION OF COPPER TRANSPORTER 1 INDUCES COGNITIVE AND EMOTIONAL ALTERATIONS THROUGH MITOCHONDRIAL DYSFUNCTION IN MICE

SUSCEPTIBILITY OF DOPAMINERGIC NERVE TERMINALS TO MITOCHONDRIAL DYSFUNCTION

LOW-INTENSITY PULSED ULTRASOUND PROTECTS RETINAL GANGLION CELLS FROM GLUTAMATE-INDUCED MITOCHONDRIAL DYSFUNCTION AND NEURONAL INJURY

MITOCHONDRIAL DYSFUNCTION SHAPES CEREBELLUM MECHANICS, NEUROINFLAMMATION, AND METABOLIC IMBALANCE: INSIGHTS FROM THE HARLEQUIN MOUSE

MULTI-OMICS CHARACTERIZATION OF TELOMERASE DEFICIENT MICE REVEALED MITOCHONDRIAL DYSFUNCTION AS A HALLMARK OF BRAIN SENESCENCE

INVESTIGATING SIAH2-E3 LIGASE ACTIVATION AND MITOCHONDRIAL DYSFUNCTION IN FAMILIAL AND SPORADIC MODELS OF PARKINSON’S DISEASE

Α-SYNUCLEIN OLIGOMERS INDUCE MITOCHONDRIAL DYSFUNCTION AND TRIGGER EXTRACELLULAR MITOCHONDRIAL RELEASE: IMPLICATIONS FOR ASTROCYTE-NEURON CROSSTALK

TRPV1-MEDIATED CALCIUM OVERLOAD TRIGGERS MITOCHONDRIAL DYSFUNCTION AND NEURONAL APOPTOSIS IN NEUROPATHIC PAIN

APPLICATION OF NON-INVASIVE PRENATAL SCREENING FOR MULTIPLE MITOCHONDRIAL DYSFUNCTION SYNDROME TYPE 3

NR2F1 DEFICIENCY CAUSES NEURONAL MITOCHONDRIAL DYSFUNCTION ACROSS MOUSE AND HUMAN MODELS OF THE NEURODEVELOPMENTAL DISORDER BBSOAS

Contribution of cGAS-P2X2 crosstalk on synaptic failure and mitochondrial dysfunction induced by β-amyloid oligomers

Exploring the impact of transglutaminase 2 in Parkinson’s disease: Mitochondrial dysfunction and proteomic pathways

From systems biology to drug targets: ATP synthase subunit upregulation causes mitochondrial dysfunction in Shank3Δ4-22 mouse model of autism

The interplay between oxidative stress, mitochondrial dysfunction, and alteration of parvalbumin interneurons in postmortem brain of Alzheimer’s disease and mild cognitive impairment patients

Investigating the role of Rab proteins in mitochondrial dysfunction related to Parkinson’s disease

Mitochondrial dysfunction and Purkinje cell loss in Christianson syndrome

Mitochondrial dysfunction underlies impaired neurovascular coupling following traumatic brain injury

A novel perspective: Early-life stress at the origin of AD-related mitochondrial dysfunctions

Alterations in WWOX protein and gene lead to mitochondrial dysfunction in amyotrophic lateral sclerosis

Gestational stress induces mitochondrial dysfunction in prefrontal cortex and depressive-like behavior in postpartum rats

Mir-34 family is involved in Chronic Social Defeat-induced vulnerability to mood disorders and cardiac mitochondrial dysfunctions

Mitochondrial dysfunction and depression : the chicken or the egg ?

Mitochondrial dysfunction in Rett syndrome mice models: studying a neurological disorder from synaptic metabolism perspective to find new treatment options

Naringenin modulates paraquat-induced oxidative stress and mitochondrial dysfunction in a cellular model of Parkinson’s disease (SH-SY5Y cells)

The role of mitochondrial dysfunction in cellular senescence and Alzheimer’s disease-related amyloid pathology

Unravelling the role of CHCHD2 in mitochondrial dysfunction: Implications for Parkinson's disease and beyond

Sirtuins Modulators Counteract Mitochondrial Dysfunction In Chemical And Neonatal Hypoxia: Implication To Neurodevelopmental Disorders

Treatment with the CB1R antagonist rimonabant rescues brain mitochondrial dysfunction via inhibition of intra-mitochondrial protein kinase A signalling in a mouse model of Rett syndrome