Neural connections, mental computation

1993 ◽  
Vol 62 (1) ◽  
pp. 141-151
Author(s):  
Benjamin Martin
1990 ◽  
Vol 30 (2) ◽  
pp. 189-191
Author(s):  
Noel Sharkey

2020 ◽  
Author(s):  
Jonathan Sanching Tsay ◽  
Carolee Winstein

Neurorehabilitation relies on core principles of neuroplasticity to activate and engage latent neural connections, promote detour circuits, and reverse impairments. Clinical interventions incorporating these principles have been shown to promote recovery while demoting compensation. However, many clinicians struggle to find evidence for these principles in our growing but nascent body of literature. Regulatory bodies and organizational balance sheets further discourage evidence-based, methodical, time-intensive, and efficacious interventions because practical needs often outweigh and dominate clinical decision making. Modern neurorehabilitation practices that result from these pressures favor strategies that encourage compensation over those that promote recovery. With a focus on helping the busy clinician evaluate the rapidly growing literature, we put forth five simple rules that direct clinicians toward intervention studies that value more enduring but slower biological recovery processes over the more alluring practical and immediate “recovery” mantra. Filtering emerging literature through this critical lens has the potential to change practice and lead to more durable long-term outcomes. This perspective is meant to serve a new generation of mechanistically minded clinicians, students, and trainees poised to not only advance our field but to also erect policy changes that promote recovery-based care of stroke survivors.


2021 ◽  
Vol 11 (5) ◽  
pp. 663
Author(s):  
Elena D. Bazhanova ◽  
Alexander A. Kozlov ◽  
Anastasia V. Litovchenko

Epilepsy is a chronic neurological disorder characterized by recurring spontaneous seizures. Drug resistance appears in 30% of patients and it can lead to premature death, brain damage or a reduced quality of life. The purpose of the study was to analyze the drug resistance mechanisms, especially neuroinflammation, in the epileptogenesis. The information bases of biomedical literature Scopus, PubMed, Google Scholar and SciVerse were used. To obtain full-text documents, electronic resources of PubMed Central and Research Gate were used. The article examines the recent research of the mechanisms of drug resistance in epilepsy and discusses the hypotheses of drug resistance development (genetic, epigenetic, target hypothesis, etc.). Drug-resistant epilepsy is associated with neuroinflammatory, autoimmune and neurodegenerative processes. Neuroinflammation causes immune, pathophysiological, biochemical and psychological consequences. Focal or systemic unregulated inflammatory processes lead to the formation of aberrant neural connections and hyperexcitable neural networks. Inflammatory mediators affect the endothelium of cerebral vessels, destroy contacts between endothelial cells and induce abnormal angiogenesis (the formation of “leaky” vessels), thereby affecting the blood–brain barrier permeability. Thus, the analysis of pro-inflammatory and other components of epileptogenesis can contribute to the further development of the therapeutic treatment of drug-resistant epilepsy.


Cells ◽  
2019 ◽  
Vol 8 (8) ◽  
pp. 883 ◽  
Author(s):  
Debajyoti Chowdhury ◽  
Chao Wang ◽  
Ai-Ping Lu ◽  
Hai-Long Zhu

Circadian rhythms have a deep impact on most aspects of physiology. In most organisms, especially mammals, the biological rhythms are maintained by the indigenous circadian clockwork around geophysical time (~24-h). These rhythms originate inside cells. Several core components are interconnected through transcriptional/translational feedback loops to generate molecular oscillations. They are tightly controlled over time. Also, they exert temporal controls over many fundamental physiological activities. This helps in coordinating the body’s internal time with the external environments. The mammalian circadian clockwork is composed of a hierarchy of oscillators, which play roles at molecular, cellular, and higher levels. The master oscillation has been found to be developed at the hypothalamic suprachiasmatic nucleus in the brain. It acts as the core pacemaker and drives the transmission of the oscillation signals. These signals are distributed across different peripheral tissues through humoral and neural connections. The synchronization among the master oscillator and tissue-specific oscillators offer overall temporal stability to mammals. Recent technological advancements help us to study the circadian rhythms at dynamic scale and systems level. Here, we outline the current understanding of circadian clockwork in terms of molecular mechanisms and interdisciplinary concepts. We have also focused on the importance of the integrative approach to decode several crucial intricacies. This review indicates the emergence of such a comprehensive approach. It will essentially accelerate the circadian research with more innovative strategies, such as developing evidence-based chronotherapeutics to restore de-synchronized circadian rhythms.


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