scholarly journals Vesicular dysfunction and pathways to neurodegeneration

2021 ◽  
Author(s):  
Patrick A. Lewis

Abstract Cellular control of vesicle biology and trafficking is critical for cell viability, with disruption of these pathways within the cells of the central nervous system resulting in neurodegeneration and disease. The past two decades have provided important insights into both the genetic and biological links between vesicle trafficking and neurodegeneration. In this essay, the pathways that have emerged as being critical for neuronal survival in the human brain will be discussed – illustrating the diversity of proteins and cellular events with three molecular case studies drawn from different neurological diseases.

Author(s):  
Konstantin Gulyabin

Mills' syndrome is a rare neurological disorder. Its nosological nature is currently not completely determined. Nevertheless, Mills' syndrome is considered to be a rare variant of the degenerative pathology of the central nervous system – a variant of focal cortical atrophy. The true prevalence of this pathology is unknown, since this condition is more often of a syndrome type, observed in the clinical picture of a number of neurological diseases (primary lateral sclerosis, frontotemporal dementia, etc.) and is less common in isolated form.


CNS Spectrums ◽  
2005 ◽  
Vol 10 (4) ◽  
pp. 298-308 ◽  
Author(s):  
Walter Zieglgänsberger ◽  
Achim Berthele ◽  
Thomas R. Tölle

AbstractNeuropathic pain is defined as a chronic pain condition that occurs or persists after a primary lesion or dysfunction of the peripheral or central nervous system. Traumatic injury of peripheral nerves also increases the excitability of nociceptors in and around nerve trunks and involves components released from nerve terminals (neurogenic inflammation) and immunological and vascular components from cells resident within or recruited into the affected area. Action potentials generated in nociceptors and injured nerve fibers release excitatory neurotransmitters at their synaptic terminals such as L-glutamate and substance P and trigger cellular events in the central nervous system that extend over different time frames. Short-term alterations of neuronal excitability, reflected for example in rapid changes of neuronal discharge activity, are sensitive to conventional analgesics, and do not commonly involve alterations in activity-dependent gene expression. Novel compounds and new regimens for drug treatment to influence activity-dependent long-term changes in pain transducing and suppressive systems (pain matrix) are emerging.


2021 ◽  
Vol 13 ◽  
Author(s):  
Banglian Hu ◽  
Shengshun Duan ◽  
Ziwei Wang ◽  
Xin Li ◽  
Yuhang Zhou ◽  
...  

The colony-stimulating factor 1 receptor (CSF1R) is a key tyrosine kinase transmembrane receptor modulating microglial homeostasis, neurogenesis, and neuronal survival in the central nervous system (CNS). CSF1R, which can be proteolytically cleaved into a soluble ectodomain and an intracellular protein fragment, supports the survival of myeloid cells upon activation by two ligands, colony stimulating factor 1 and interleukin 34. CSF1R loss-of-function mutations are the major cause of adult-onset leukoencephalopathy with axonal spheroids and pigmented glia (ALSP) and its dysfunction has also been implicated in other neurodegenerative disorders including Alzheimer’s disease (AD). Here, we review the physiological functions of CSF1R in the CNS and its pathological effects in neurological disorders including ALSP, AD, frontotemporal dementia and multiple sclerosis. Understanding the pathophysiology of CSF1R is critical for developing targeted therapies for related neurological diseases.


2021 ◽  
Vol 20 (5) ◽  
pp. 500-508
Author(s):  
G. V. Pervushin

Despite the enormous incidence of malaria over the past 2 years, complications of this disease from the nervous system are relatively rare.


2021 ◽  
Vol 11 ◽  
Author(s):  
Lintao Wang ◽  
Zhiguang Ren ◽  
Li Ma ◽  
Yanjie Han ◽  
Wenqiang Wei ◽  
...  

COVID-19 has spread rapidly worldwide since its outbreak and has now become a major public health problem. More and more evidence indicates that SARS-CoV-2 may not only affect the respiratory system but also cause great harm to the central nervous system. Therefore, it is extremely important to explore in-depth the impact of SARS-CoV-2 infection on the nervous system. In this paper, the possible mechanisms of SARS-CoV-2 invading the central nervous system during COVID-19, and the neurological complications caused by SARS-CoV-2 infection were reviewed.


Physiology ◽  
2003 ◽  
Vol 18 (3) ◽  
pp. 109-114 ◽  
Author(s):  
Anthony R. Hobson ◽  
Qasim Aziz

To understand the pathophysiology of anomalous pain in functional gastrointestinal disorders, we must increase our understanding of how the central nervous system processes visceral pain. Over the past decade, novel application of functional brain imaging and electrophysiological techniques has given us the opportunity to study these processes in humans, and this review summarizes the current body of knowledge.


2015 ◽  
Vol 20 (2) ◽  
pp. 125-149 ◽  
Author(s):  
Orly Lewis ◽  
Pavel Gregoric

This paper underlines the importance of the Pseudo-Aristotelian treatise De spiritu for our knowledge of early Hellenistic anatomical and physiological theories. We claim that the treatise verifies reports on certain 4th- and 3rd-century conceptions and debates otherwise attested only in later sources, and offers invaluable information on otherwise unknown ideas and discussions. Our claim is based on ten case-studies in which we explore the relation between the views found in De spiritu and known to us from other ancient sources, regarding ten specific topics. Following the results of our case-studies, we argue that De spiritu should be dated to the early decades of the 3rd century bc, after the circulation of the doctrines of Praxagoras of Cos, but before the discovery of the central nervous system by Herophilus and Erasistratus.



Endocrinology ◽  
2013 ◽  
Vol 154 (9) ◽  
pp. 3001-3007 ◽  
Author(s):  
Julie A. Chowen ◽  
Jesús Argente ◽  
Tamas L. Horvath

Glial cells, which constitute more than 50% of the mass of the central nervous system and greatly outnumber neurons, are at the vanguard of neuroendocrine research in metabolic control and obesity. Historically relegated to roles of structural support and protection, diverse functions have been gradually attributed to this heterogeneous class of cells with their protagonism in crescendo in all areas of neuroscience during the past decade. However, this dramatic increase in attention bestowed upon glial cells has also emphasized our vast lack of knowledge concerning many aspects of their physiological functions, let alone their participation in numerous pathologies. This minireview focuses on the recent advances in our understanding of how glial cells participate in the physiological regulation of appetite and systemic metabolism as well as their role in the pathophysiological response to poor nutrition and secondary complications associated with obesity. Moreover, we highlight some of the existing lagoons of knowledge in this increasingly important area of investigation.


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