Coenzyme Q10 treatment ameliorates cognitive deficits by modulating mitochondrial functions in surgically induced menopause

2014 ◽  
Vol 74 ◽  
pp. 16-23 ◽  
Author(s):  
Rajat Sandhir ◽  
Neha Sethi ◽  
Aanchal Aggarwal ◽  
Alka Khera
Keyword(s):  
Cognitive Deficits ◽  
Coenzyme Q10 ◽  
Mitochondrial Functions ◽  
Surgically Induced

The protective effect of coenzyme Q10 and berberine on sperm parameters, with and without varicocelectomy in rats with surgically induced varicoceles

2018 ◽  
Vol 28 (2) ◽  
pp. 479-485 ◽  
Author(s):  
Hamed Najaran ◽  
Hamid Rashtbari ◽  
Abouzar Mohammadi ◽  
Fatemeh Soleimanifar ◽  
Fatemeh Izadpanah ◽  
...  
Keyword(s):  
Protective Effect ◽  
Coenzyme Q10 ◽  
Sperm Parameters ◽  
Surgically Induced

scholarly journals Dysfunction in nonsense-mediated decay, protein homeostasis, mitochondrial function, and brain connectivity in ALS-FUS mice with cognitive deficits

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Wan Yun Ho ◽  
Ira Agrawal ◽  
Sheue-Houy Tyan ◽  
Emma Sanford ◽  
Wei-Tang Chang ◽  
...  
Keyword(s):  
Cognitive Deficits ◽  
Brain Connectivity ◽  
Expression Patterns ◽  
Long Term Potentiation ◽  
Protein Homeostasis ◽  
Spine Density ◽  
Nonsense Mediated Decay ◽  
Endogenous Expression ◽  
Mitochondrial Functions

AbstractAmyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) represent two ends of the same disease spectrum of adult-onset neurodegenerative diseases that affect the motor and cognitive functions, respectively. Multiple common genetic loci such as fused in sarcoma (FUS) have been identified to play a role in ALS and FTD etiology. Current studies indicate that FUS mutations incur gain-of-toxic functions to drive ALS pathogenesis. However, how the disease-linked mutations of FUS affect cognition remains elusive. Using a mouse model expressing an ALS-linked human FUS mutation (R514G-FUS) that mimics endogenous expression patterns, we found that FUS proteins showed an age-dependent accumulation of FUS proteins despite the downregulation of mouse FUS mRNA by the R514G-FUS protein during aging. Furthermore, these mice developed cognitive deficits accompanied by a reduction in spine density and long-term potentiation (LTP) within the hippocampus. At the physiological expression level, mutant FUS is distributed in the nucleus and cytosol without apparent FUS aggregates or nuclear envelope defects. Unbiased transcriptomic analysis revealed a deregulation of genes that cluster in pathways involved in nonsense-mediated decay, protein homeostasis, and mitochondrial functions. Furthermore, the use of in vivo functional imaging demonstrated widespread reduction in cortical volumes but enhanced functional connectivity between hippocampus, basal ganglia and neocortex in R514G-FUS mice. Hence, our findings suggest that disease-linked mutation in FUS may lead to changes in proteostasis and mitochondrial dysfunction that in turn affect brain structure and connectivity resulting in cognitive deficits.

scholarly journals Neuroprotective effect of hesperidin and its combination with coenzyme Q10 on an animal model of ketamine-induced psychosis: behavioral changes, mitochondrial dysfunctions, and oxidative stress

2022 ◽  
Vol 8 (1) ◽  
Author(s):  
Naresh Kumar ◽  
Monu Yadav ◽  
Anil Kumar ◽  
Monika Kadian ◽  
Sunil Kumar
Keyword(s):  
Locomotor Activity ◽  
Side Effects ◽  
Coenzyme Q10 ◽  
Negative Symptoms ◽  
Behavioral Changes ◽  
Psychotic Symptoms ◽  
Positive Symptoms ◽  
Immobility Duration ◽  
Olanzapine Treatment ◽  
Mitochondrial Functions

Abstract Background Psychosis is a complex mental illness divided by positive symptoms, negative symptoms, and cognitive decline. Clinically available medicines are associated with some serious side effects which limit their use. Treatment with flavonoids has been associated with delayed onset and development, decreased risk, or increased improvement of various neuropsychiatric disorders including psychosis with negligible side effects. Therefore, the present study was aimed to investigate the protective effects of hesperidin (flavonoid) alone or its combination with coenzyme Q10 against ketamine-induced psychotic symptoms in mice. Results Ketamine (50 mg/kg, i.p.) was given for 21 days to induce psychosis in Laca mice of either sex. Locomotor activity and stereotypic behaviors, immobility duration (forced swim test), and increased transfer latency (elevated plus maze) were performed to test the effect of hesperidin (50 mg/kg, 100 mg/kg, 200 mg/kg, p.o.) and coenzyme Q10 (20 mg/kg, 40 mg/kg, p.o.) and combination of hesperidin + coenzyme Q10 followed by biochemical and mitochondrial complexes assays. For 21 days, ketamine (50 mg/kg, i.p.) administration significantly produced increased locomotor activity and stereotypic behaviors (positive symptoms), increased immobility duration (negative symptoms) and cognitive deficits (increases transfer latency) weakens oxidative defense and mitochondrial function. Further, 21 days’ administration of hesperidin and coenzyme Q10 significantly reversed the ketamine-induced psychotic behavioral changes and biochemical alterations and mitochondrial dysfunction in the discrete areas (prefrontal cortex and hippocampus) of mice brains. The potential effect of these drugs was comparable to olanzapine treatment. Moreover, the combination of hesperidin with coenzyme Q10 and or a combination of hesperidin + coenzyme Q10 + olanzapine treatment did not produce a significant effect compared to their per se effect in ketamine-treated animals. Conclusions The study revealed that hesperidin alone or in combination with coenzyme Q10 could reduce psychotic symptoms and improve mitochondrial functions and antioxidant systems in mice, suggesting neuroprotective effects against psychosis.

scholarly journals Insights into Disease-Associated Tau Impact on Mitochondria

2020 ◽  
Vol 21 (17) ◽  
pp. 6344 ◽  
Author(s):  
Leonora Szabo ◽  
Anne Eckert ◽  
Amandine Grimm
Keyword(s):  
Cognitive Deficits ◽  
Tau Protein ◽  
Frontotemporal Lobar Degeneration ◽  
Therapeutic Interventions ◽  
Mitochondrial Proteins ◽  
Early Event ◽  
Substantial Evidence ◽  
Mitochondrial Functions ◽  
Underlying Mechanisms ◽  
The Brain

Abnormal tau protein aggregation in the brain is a hallmark of tauopathies, such as frontotemporal lobar degeneration and Alzheimer’s disease. Substantial evidence has been linking tau to neurodegeneration, but the underlying mechanisms have yet to be clearly identified. Mitochondria are paramount organelles in neurons, as they provide the main source of energy (adenosine triphosphate) to these highly energetic cells. Mitochondrial dysfunction was identified as an early event of neurodegenerative diseases occurring even before the cognitive deficits. Tau protein was shown to interact with mitochondrial proteins and to impair mitochondrial bioenergetics and dynamics, leading to neurotoxicity. In this review, we discuss in detail the different impacts of disease-associated tau protein on mitochondrial functions, including mitochondrial transport, network dynamics, mitophagy and bioenergetics. We also give new insights about the effects of abnormal tau protein on mitochondrial neurosteroidogenesis, as well as on the endoplasmic reticulum-mitochondria coupling. A better understanding of the pathomechanisms of abnormal tau-induced mitochondrial failure may help to identify new targets for therapeutic interventions.

scholarly journals Neuroprotective Effect of Clobenpropit against Lipopolysaccharide-Induced Cognitive Deficits via Attenuating Neuroinflammation and Enhancing Mitochondrial Functions in Mice

2021 ◽  
Vol 11 (12) ◽  
pp. 1617
Author(s):  
Vasudevan Mani ◽  
Minhajul Arfeen ◽  
Hussein M. Ali ◽  
Abdel-Moneim Hafez Abdel-Moneim ◽  
Maha Aldubayan ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Cognitive Deficits ◽  
Neuroprotective Effect ◽  
Neuronal Cell ◽  
Chain Complex ◽  
Neuronal Necrosis ◽  
Memory Error ◽  
Mitochondrial Respiratory Chain Complex ◽  
Mitochondrial Functions ◽  
Tgf Β1

Clobenpropit (CLO), an antagonist on histamine H3 receptors (HH3R), has been shown to protect NMDA-induced neuronal necrosis in cortical neuronal cell culture from rats. In this work, we explored its potential on lipopolysaccharide (LPS)-induced memory deficits, neuroinflammation, and mitochondrial dysfunction in mice. CLO (1 and 3 mg/kg, p.o.) was treated continually for 30 days, and neurotoxicity was induced by four doses of LPS (250 µg/kg, i.p.). The radial arm maze (RAM) was used to access memory behaviors. After the REM test, brain tissue was collected from each mouse to estimate pro-inflammatory cytokines (TNFα and IL6), anti-inflammatory cytokines (TGF-β1 and IL-10), cyclooxygenase-2 (COX 2), and mitochondrial respiratory chain complex (MRCC- I, II and IV) enzymes. CLO treatment reversed the LPS-induced behavioral deficits by a significant reduction in time taken to consume all five bites (TTB), working memory error (WME), and reference memory error (REM) in the REM test. Regarding neuroinflammation, it attenuated the release of COX, TNF-α, and IL-6, and augmented TGF-β1 and IL-10 levels in the brain. Reversal of LPS-induced brain MRCC (I, II, and IV) levels also resulted with CLO treatment. From these findings, CLO promises neuroprotection against LPS-induced cognitive deficits by ameliorating neuroinflammation and restoring the MRCC enzymes in mice.

No Cognitive Deficits in Preeclamptics on MgSO4

Ob Gyn News ◽  
2005 ◽  
Vol 40 (2) ◽  
pp. 20
Author(s):  
MIRIAM E. TUCKER
Keyword(s):  
Cognitive Deficits

Topographische Orientierung bei Patienten mit erworbener Hirnschädigung

1999 ◽  
Vol 10 (2) ◽  
pp. 77-86
Author(s):  
Martina Kindsmüller ◽  
Andrea Kaindl ◽  
Uwe Schuri ◽  
Alf Zimmer
Keyword(s):  
Brain Damage ◽  
Cognitive Deficits ◽  
Hospital Setting ◽  
Hospital Staff ◽  
Reading Test ◽  
Map Reading ◽  
Several Variables ◽  
Topographical Orientation ◽  
The One ◽  
Behavioral Memory

Topographical Orientation in Patients with Acquired Brain Damage Abstract: A study was conducted to investigate the abilities of topographical orientation in patients with acquired brain damage. The first study investigates the correlation between wayfinding in a hospital setting and various sensory and cognitive deficits as well as the predictability of navigating performance by specific tests, self-rating of orientation ability and rating by staff. The investigation included 35 neuropsychological patients as well as 9 control subjects. Several variables predicted the wayfinding performance reasonably well: memory tests like the one introduced by Muramoto and a subtest of the Rivermead Behavioral Memory Test, the Map Reading Test and the rating by hospital staff. Patients with hemianopia experienced significant difficulty in the task.

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