Hope and the brain: Trait hope mediates the protective role of medial orbitofrontal cortex spontaneous activity against anxiety

NeuroImage ◽  
2017 ◽  
Vol 157 ◽  
pp. 439-447 ◽  
Author(s):  
Song Wang ◽  
Xin Xu ◽  
Ming Zhou ◽  
Taolin Chen ◽  
Xun Yang ◽  
...  
Keyword(s):  
Spontaneous Activity ◽  
Orbitofrontal Cortex ◽  
Protective Role ◽  
Trait Hope ◽  
The Brain

scholarly journals Optimism and the brain: trait optimism mediates the protective role of the orbitofrontal cortex gray matter volume against anxiety

2015 ◽  
Vol 11 (2) ◽  
pp. 263-271 ◽  
Author(s):  
Sanda Dolcos ◽  
Yifan Hu ◽  
Alexandru D. Iordan ◽  
Matthew Moore ◽  
Florin Dolcos
Keyword(s):  
Gray Matter ◽  
Orbitofrontal Cortex ◽  
Gray Matter Volume ◽  
Protective Role ◽  
Matter Volume ◽  
The Brain

scholarly journals Serum Amyloid Beta42 Is Not Eliminated by the Cirrhotic Liver: A Pilot Study

2021 ◽  
Vol 10 (12) ◽  
pp. 2669
Author(s):  
Reiner Wiest ◽  
Thomas S. Weiss ◽  
Lusine Danielyan ◽  
Christa Buechler
Keyword(s):  
Liver Cirrhosis ◽  
Hepatic Clearance ◽  
Protective Role ◽  
Tissue Growth ◽  
Cirrhotic Liver ◽  
Diabetic Patients ◽  
Peripheral Clearance ◽  
End Stage ◽  
The Brain

Amyloid-beta (Aβ) deposition in the brain is the main pathological hallmark of Alzheimer disease. Peripheral clearance of Aβ may possibly also lower brain levels. Recent evidence suggested that hepatic clearance of Aβ42 is impaired in liver cirrhosis. To further test this hypothesis, serum Aβ42 was measured by ELISA in portal venous serum (PVS), systemic venous serum (SVS), and hepatic venous serum (HVS) of 20 patients with liver cirrhosis. Mean Aβ42 level was 24.7 ± 20.4 pg/mL in PVS, 21.2 ± 16.7 pg/mL in HVS, and 19.2 ± 11.7 pg/mL in SVS. Similar levels in the three blood compartments suggested that the cirrhotic liver does not clear Aβ42. Aβ42 was neither associated with the model of end-stage liver disease score nor the Child–Pugh score. Patients with abnormal creatinine or bilirubin levels or prolonged prothrombin time did not display higher Aβ42 levels. Patients with massive ascites and patients with large varices had serum Aβ42 levels similar to patients without these complications. Serum Aβ42 was negatively associated with connective tissue growth factor levels (r = −0.580, p = 0.007) and a protective role of Aβ42 in fibrogenesis was already described. Diabetic patients with liver cirrhosis had higher Aβ42 levels (p = 0.069 for PVS, p = 0.047 for HVS and p = 0.181 for SVS), which is in accordance with previous reports. Present analysis showed that the cirrhotic liver does not eliminate Aβ42. Further studies are needed to explore the association of liver cirrhosis, Aβ42 levels, and cognitive dysfunction.

scholarly journals Genetic Variants of Lipoprotein Lipase and Regulatory Factors Associated with Alzheimer’s Disease Risk

2020 ◽  
Vol 21 (21) ◽  
pp. 8338
Author(s):  
Kimberley D. Bruce ◽  
Maoping Tang ◽  
Philip Reigan ◽  
Robert H. Eckel
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Lipoprotein Lipase ◽  
Genetic Variants ◽  
Disease Risk ◽  
Lipoprotein Metabolism ◽  
Protective Role ◽  
Direct Role ◽  
The Brain

Lipoprotein lipase (LPL) is a key enzyme in lipid and lipoprotein metabolism. The canonical role of LPL involves the hydrolysis of triglyceride-rich lipoproteins for the provision of FFAs to metabolic tissues. However, LPL may also contribute to lipoprotein uptake by acting as a molecular bridge between lipoproteins and cell surface receptors. Recent studies have shown that LPL is abundantly expressed in the brain and predominantly expressed in the macrophages and microglia of the human and murine brain. Moreover, recent findings suggest that LPL plays a direct role in microglial function, metabolism, and phagocytosis of extracellular factors such as amyloid- beta (Aβ). Although the precise function of LPL in the brain remains to be determined, several studies have implicated LPL variants in Alzheimer’s disease (AD) risk. For example, while mutations shown to have a deleterious effect on LPL function and expression (e.g., N291S, HindIII, and PvuII) have been associated with increased AD risk, a mutation associated with increased bridging function (S447X) may be protective against AD. Recent studies have also shown that genetic variants in endogenous LPL activators (ApoC-II) and inhibitors (ApoC-III) can increase and decrease AD risk, respectively, consistent with the notion that LPL may play a protective role in AD pathogenesis. Here, we review recent advances in our understanding of LPL structure and function, which largely point to a protective role of functional LPL in AD neuropathogenesis.

scholarly journals Canadian Association of Neurosciences Review: Postnatal Development of the Mammalian Neocortex: Role of Activity Revisited

2006 ◽  
Vol 33 (2) ◽  
pp. 158-169 ◽  
Author(s):  
Zhong-wei Zhang
Keyword(s):  
Spontaneous Activity ◽  
Brain Function ◽  
Postnatal Life ◽  
Synaptic Connections ◽  
Synaptic Remodeling ◽  
Canadian Association ◽  
Selective Elimination ◽  
Neuronal Connections ◽  
The Brain

ABSTRACT:The mammalian neocortex is the largest structure in the brain, and plays a key role in brain function. A critical period for the development of the neocortex is the early postnatal life, when the majority of synapses are formed and when much of synaptic remodeling takes place. Early studies suggest that initial synaptic connections lack precision, and this rudimentary wiring pattern is refined by experience-related activity through selective elimination and consolidation. This view has been challenged by recent studies revealing the presence of a relatively precise pattern of connections before the onset of sensory experience. The recent data support a model in which specificity of neuronal connections is largely determined by genetic factors. Spontaneous activity is required for the formation of neural circuits, but whether it plays an instructive role is still controversial. Neurotransmitters including acetylcholine, serotonin, and γ-Aminobutyric acid (GABA) may have key roles in the regulation of spontaneous activity, and in the maturation of synapses in the developing brain.

Physical activity as a protective factor for successful aging

2019 ◽  
Vol 29 (87) ◽  
pp. 47-52
Author(s):  
Andrzej Jopkiewicz ◽  
Monika Królicka–Czerniak ◽  
Anita Zaręba
Keyword(s):  
Physical Activity ◽  
Prefrontal Cortex ◽  
Cognitive Processes ◽  
Cognitive Aging ◽  
Successful Aging ◽  
Protective Factor ◽  
Protective Role ◽  
Factors Affecting ◽  
The Brain

To divide the types of aging (successful, usual and impaired), as well as factors affecting this process, the protective role of physical activity was discussed in the literature. It was emphasized that physical activity is also a very important protective factor for cognitive aging - mainly executive function and memory. The prefrontal cortex and hippocampus, i.e. the regions of the brain responsible for the control and course of cognitive processes, show susceptibility to stimulation, which is movement exercises, which are prevention of degenerative changes within the brain.

scholarly journals Value Representations in the Rodent Orbitofrontal Cortex Drive Learning, not Choice

2018 ◽  
Author(s):  
Kevin J. Miller ◽  
Matthew M. Botvinick ◽  
Carlos D. Brody
Keyword(s):  
Orbitofrontal Cortex ◽  
Future Expectations ◽  
Neural Representations ◽  
Electrophysiological Recordings ◽  
Expected Values ◽  
Open Question ◽  
Reward Information ◽  
To Receive ◽  
The Brain

AbstractHumans and animals make predictions about the rewards they expect to receive in different situations. In formal models of behavior, these predictions are known as value representations, and they play two very different roles. Firstly, they drive choice: the expected values of available options are compared to one another, and the best option is selected. Secondly, they support learning: expected values are compared to rewards actually received, and future expectations are updated accordingly. Whether these different functions are mediated by different neural representations remains an open question. Here we employ a recently-developed multi-step task for rats that computationally separates learning from choosing. We investigate the role of value representations in the rodent orbitofrontal cortex, a key structure for value-based cognition. Electrophysiological recordings and optogenetic perturbations indicate that these representations do not directly drive choice. Instead, they signal expected reward information to a learning process elsewhere in the brain that updates choice mechanisms.

scholarly journals Melatonin and Ischemic Stroke: Mechanistic Roles and Action

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Syed Suhail Andrabi ◽  
Suhel Parvez ◽  
Heena Tabassum
Keyword(s):  
Ischemic Stroke ◽  
Brain Injury ◽  
Neurological Diseases ◽  
Neuroprotective Effect ◽  
Economic Loss ◽  
Protective Role ◽  
Physiological Processes ◽  
Cord Injury ◽  
The Brain

Stroke is one of the most devastating neurological disabilities and brain’s vulnerability towards it proves to be fatal and socio-economic loss of millions of people worldwide. Ischemic stroke remains at the center stage of it, because of its prevalence amongst the several other types attacking the brain. The various cascades of events that have been associated with stroke involve oxidative stress, excitotoxicity, mitochondrial dysfunction, upregulation of Ca2+level, and so forth. Melatonin is a neurohormone secreted by pineal and extra pineal tissues responsible for various physiological processes like sleep and mood behaviour. Melatonin has been implicated in various neurological diseases because of its antioxidative, antiapoptotic, and anti-inflammatory properties. We have previously reviewed the neuroprotective effect of melatonin in various models of brain injury like traumatic brain injury and spinal cord injury. In this review, we have put together the various causes and consequence of stroke and protective role of melatonin in ischemic stroke.

Minireview: Cell protective role of melatonin in the brain

1995 ◽  
Vol 19 (2) ◽  
pp. 57-63 ◽  
Author(s):  
Darfo Acufla-Castroviejo ◽  
Germaine Escames ◽  
Manuel Macks ◽  
Antono Muñóz Hoyos ◽  
Antonio Molina Carballo ◽  
...  
Keyword(s):  
Protective Role ◽  
The Brain

scholarly journals Protective Role of rAAV-NDI1, Serotype 5, in an Acute MPTP Mouse Parkinson's Model

2011 ◽  
Vol 2011 ◽  
pp. 1-10 ◽  
Author(s):  
Jennifer Barber-Singh ◽  
Byoung Boo Seo ◽  
Akemi Matsuno-Yagi ◽  
Takao Yagi
Keyword(s):  
Complex I ◽  
Protective Role ◽  
Proton Pumping ◽  
Hereditary Diseases ◽  
Quinone Oxidoreductase ◽  
Leigh’S Syndrome ◽  
Nadh Ubiquinone Oxidoreductase ◽  
Serotype 5 ◽  
The Brain

Defects in mitochondrial proton-translocating NADH-quinone oxidoreductase (complex I) have been implicated in a number of acquired and hereditary diseases including Leigh's syndrome and more recently Parkinson's disease. A limited number of strategies have been attempted to repair the damaged complex I with little or no success. We have recently shown that the non-proton-pumping, internal NADH-ubiquinone oxidoreductase (Ndi1) fromSaccharomyces cerevisiae(baker's yeast) can be successfully inserted into the mitochondria of mice and rats, and the enzyme was found to be fully active. Using recombinant adenoassociated virus vectors (serotype 5) carrying ourNDI1gene, we were able to express the Ndi1 protein in the substantia nigra (SN) of C57BL/6 mice with an expression period of two months. The results show that the AAV serotype 5 was highly efficient in expressing Ndi1 in the SN, when compared to a previous model using serotype 2, which led to nearly 100% protection when using an acute MPTP model. It is conceivable that the AAV-serotype5 carrying theNDI1gene is a powerful tool for proof-of-concept study to demonstrate complex I defects as the causable factor in diseases of the brain.

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