neural dysfunction
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Cancers ◽  
2021 ◽  
Vol 13 (16) ◽  
pp. 3990
Author(s):  
Brennan Olson ◽  
Parham Diba ◽  
Tetiana Korzun ◽  
Daniel L. Marks

Nearly half of cancer patients suffer from cachexia, a metabolic syndrome characterized by progressive atrophy of fat and lean body mass. This state of excess catabolism decreases quality of life, ability to tolerate treatment and eventual survival, yet no effective therapies exist. Although the central nervous system (CNS) orchestrates several manifestations of cachexia, the precise mechanisms of neural dysfunction during cachexia are still being unveiled. Herein, we summarize the cellular and molecular mechanisms of CNS dysfunction during cancer cachexia with a focus on inflammatory, autonomic and neuroendocrine processes and end with a discussion of recently identified CNS mediators of cachexia, including GDF15, LCN2 and INSL3.


2021 ◽  
Vol 10 (14) ◽  
pp. 3099
Author(s):  
Cindy Zolotoff ◽  
Laurent Bertoletti ◽  
David Gozal ◽  
Valentine Mismetti ◽  
Pascale Flandrin ◽  
...  

Obstructive sleep apnea (OSA) is characterized by repeated episodes of intermittent hypoxia (IH) and is recognized as an independent risk factor for vascular diseases that are mediated by a multitude of mechanistic pathophysiological cascades including procoagulant factors. The pro-coagulant state contributes to the development of blood clots and to the increase in the permeability of the blood–brain barrier (BBB). Such alteration of BBB may alter brain function and increase the risk of neurodegenerative diseases. We aim to provide a narrative review of the relationship between the hypercoagulable state, observed in OSA and characterized by increased coagulation factor activity, as well as platelet activation, and the underlying neural dysfunction, as related to disruption of the BBB. We aim to provide a critical overview of the existing evidence about the effect of OSA on the coagulation balance (characterized by increased coagulation factor activity and platelet activation) as on the BBB. Then, we will present the emerging data on the effect of BBB disruption on the risk of underlying neural dysfunction. Finally, we will discuss the potential of OSA therapy on the coagulation balance and the improvement of BBB.


2021 ◽  
Author(s):  
Asvin KK Lakkaraju ◽  
Silvia Sorce ◽  
Assunta Senatore ◽  
Mario Nuvolone ◽  
Jingjing Guo ◽  
...  

Although prion infections cause cognitive impairment and neuronal death, transcriptional and translational profiling shows progressive derangement within glia but surprisingly little changes within neurons. Here we expressed PrPC selectively in neurons, astrocytes or oligodendrocytes of mice. After prion infection, both astrocyte and neuron-restricted PrPC expression led to copious brain accumulation of PrPSc. As expected, neuron-restricted expression was associated with typical prion disease. However, mice with astrocyte-restricted PrPC expression experienced a normal life span, did not develop clinical disease, and did not show astro- or microgliosis. Besides confirming that PrPSc is innocuous to PrPC-deficient neurons, these results show that astrocyte-born PrPSc does not activate the extreme neuroinflammation that accompanies the onset of prion disease and precedes any molecular changes of neurons. This points to a nonautonomous mechanism by which prion-infected neurons instruct astrocytes and microglia to acquire a specific cellular state that, in turn, drives neural dysfunction.


Author(s):  
Brendan Tan ◽  
Rosita Shishegar ◽  
Govinda R. Poudel ◽  
Alex Fornito ◽  
Nellie Georgiou‐Karistianis

2020 ◽  
Vol 4 (Supplement_1) ◽  
pp. 792-792
Author(s):  
Inbal Maidan ◽  
Hagar Bernad-Elazari ◽  
Roni Hacham ◽  
Jeffrey Hausdorff ◽  
Anat Mirelman

Abstract Recent work suggests that the prefrontal cortex is recruited during complex walking as a form of cognitive compensation to maintain performance in aging and neurodegenerative diseases. Evidence from fNIRS studies is accumulating on different patient groups demonstrating the utility of this method and its sensitivity to neural dysfunction. However a direct comparison that explores the specificity of prefrontal activation patterns has not been conducted. This process is essential towards implementing the use of fNIRS at the individual level. Data collected from four different cohorts; young adults, older adults, PD patients at different stages of the disease, and patients with Multiple-Sclerosis during challenging tasks will be presented. Overlap, commonality, disparity and variability between groups and conditions will be presented and modifiers and moderators that can affect individual performance will be discussed. Understanding individual differences in fNIRS response will enhance data interpretation and promote translation of this technology to clinical care applications.


2020 ◽  
Author(s):  
Lucy Vanes ◽  
Raymond J Dolan

Several decades of neuroimaging research in psychiatry have shed light on structural and functional neural abnormalities associated with individual psychiatric disorders. However, there is increasing evidence for substantial overlap in the patterns of neural dysfunction seen across disorders, suggesting that risk for psychiatric illness may be shared across diagnostic boundaries. In this narrative review, we first evaluate recent studies investigating the neural correlates of a general psychopathology factor, thought to reflect the shared variance across common mental health symptoms. We then link insights from this research to meta-analytic evidence for shared patterns of neural dysfunction across categorical psychiatric disorders. We conclude by providing an integrative account of vulnerability to mental illness that focuses on neurodevelopmental abnormalities in the context of brain connectivity.


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