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Topic Review
Therapeutic of Valproic Acid Metabolites ant Its Role
Valproic acid (CH3CH2CH2)2CHCOOH 2-propylvaleric acid, VPA) is a fatty acid derivative originally synthesized. Valproic acid (VPA) and its salts are psychotropic drugs that are widely used in neurological diseases (epilepsy, neuropathic pain, migraine, etc.) and psychiatric disorders (schizophrenia, bipolar affective disorder, addiction diseases, etc.). In addition, the indications for the appointment of valproate have been expanding in recent years in connection with the study of new mechanisms of action of therapeutic and toxic metabolites of VPA in the human body. Thus, VPA is considered a component of disease-modifying therapy for multiple tumors, neurodegenerative diseases (Huntington’s disease, Parkinson’s disease, Duchenne progressive dystrophy, etc.), and human immunodeficiency syndrome. The metabolism of VPA is complex and continues to be studied. Known pathways of VPA metabolism include: β-oxidation in the tricarboxylic acid cycle (acetylation); oxidation with the participation of cytochrome P-450 isoenzymes (P-oxidation); and glucuronidation. The complex metabolism of VPA explains the diversity of its active and inactive metabolites, which have therapeutic, neutral, or toxic effects. 
  • 770
  • 03 Feb 2023
Topic Review
Botulinum Toxin in Movement Disorders
Since its initial approval in 1989 by the US Food and Drug Administration for the treatment of blepharospasm and other facial spasms, botulinum toxin (BoNT) has evolved into a therapeutic modality for a variety of neurological and non-neurological disorders. With respect to neurologic movement disorders, BoNT has been reported to be effective for the treatment of dystonia, bruxism, tremors, tics, myoclonus, restless legs syndrome, tardive dyskinesia, and a variety of symptoms associated with Parkinson’s disease. More recently, research with BoNT has expanded beyond its use as a powerful muscle relaxant and a peripherally active drug to its potential central nervous system applications in the treatment of neurodegenerative disorders. Although BoNT is the most potent biologic toxin, when it is administered by knowledgeable and experienced clinicians, it is one of the safest therapeutic agents in clinical use. The primary aim of this article is to provide an update on recent advances in BoNT research with a focus on novel applications in the treatment of movement disorders.
  • 763
  • 31 Jan 2021
Topic Review
Neuroprotection and Non-Invasive Brain Stimulation
Non-Invasive Brain Stimulation (NIBS) techniques, such as transcranial Direct Current Stimulation (tDCS) and repetitive Magnetic Transcranial Stimulation (rTMS), are well-known non-pharmacological approaches to improve both motor and non-motor symptoms in patients with neurodegenerative disorders. Their use is of particular interest especially for the treatment of cognitive impairment in Alzheimer’s Disease (AD), as well as axial disturbances in Parkinson’s (PD), where conventional pharmacological therapies show very mild and short-lasting effects. However, their ability to interfere with disease progression over time is not well understood; recent evidence suggests that NIBS may have a neuroprotective effect, thus slowing disease progression and modulating the aggregation state of pathological proteins. 
  • 760
  • 23 Nov 2022
Topic Review
Self-Esteem in Idiopathic Epilepsy
People with etiologically unknown (idiopathic) epilepsy may have their self-esteem compromised to a certain extent, particularly the females. These results validate our position that people with epilepsy are “more than their mere symptomatic illness”, and that there is a worth in capturing wider patient-reported outcomes, beyond mere seizure frequency and severity. We consider that the usual epilepsy care must go beyond the mere prescription of ASMs.
  • 758
  • 29 Oct 2020
Topic Review
Traumatic Brachial Plexus
Traumatic brachial plexus injuries are rare but serious consequences of major traumas. Pre-ganglionic lesions are considered irreparable, while post-ganglionic injuries can be potentially treated if an early diagnosis is available.
  • 758
  • 18 Feb 2021
Topic Review
Kynurenine Pathway in Neurodegeneration
The astrocytes and neuronal cells are considered to be neuroprotective, whereas the infiltrating macrophages and activated microglia are considered to be neurotoxic. Therefore, multiple products of KP can have neuroprotective, neurotoxic, and immunomodulatory effects. QUIN, an excitotoxin, is reported to be the most significant among them, which results in the death of neurons.
  • 757
  • 02 Aug 2021
Topic Review
Brain-Derived Neurotrophic Factor
Brain-derived neurotrophic factor (BDNF) is one of the most studied neurotrophins. Low BDNF concentrations have been noted in patients with traditional cardiovascular disease risk factors and have been associated with the increased risk of stroke/transient ischemic attack (TIA).
  • 755
  • 19 Apr 2021
Topic Review
Brain Insulin Resistance
Current hypotheses implicate insulin resistance of the brain as a pathogenic factor in the development of Alzheimer’s disease and other dementias, Parkinson’s disease, type 2 diabetes, obesity, major depression, and traumatic brain injury. A variety of genetic, developmental, and metabolic abnormalities that lead to disturbances in the insulin receptor signal transduction may underlie insulin resistance. Insulin receptor substrate proteins are generally considered to be the node in the insulin signaling system that is critically involved in the development of insulin insensitivity during metabolic stress, hyperinsulinemia, and inflammation. Emerging evidence suggests that lower activation of the insulin receptor (IR) is another common, while less discussed, mechanism of insulin resistance in the brain.
  • 753
  • 22 Apr 2021
Topic Review
Pathophysiology of ALS
Amyotrophic lateral sclerosis (ALS) is the most common neurodegenerative disease of the motor system. It is characterized by the degeneration of both upper and lower motor neurons, which leads to muscle weakness and paralysis. ALS is incurable and has a bleak prognosis, with median survival of 3–5 years after the initial symptomatology.
  • 748
  • 26 Jul 2021
Topic Review
MECP2-Related Disorders in Males
Methyl CpG binding protein 2 ( MECP2 ) is an unstructured protein that can adopt local secondary structures when binding to other molecules, which explains its involvement in multiple molecular interactions and thereby, functions. Thus, MECP2 is a multifunctional gene that acts as a transcriptional regulator (both activating and repressing) and a chromatin remodeler; it also interacts with the RNA splicing machinery and with microRNA processing machinery, among others. Post-translational modifications are also implicated in regulating its activity and interactions with other proteins.
  • 748
  • 08 Feb 2022
Topic Review
Monoclonal Antibodies as Neurological Therapeutics
Monoclonal antibodies are key therapeutic agents for several neurological conditions with diverse pathophysiological mechanisms, including multiple sclerosis, migraines and neuromuscular disease. In addition, a great number of monoclonal antibodies against several targets are being investigated for many more neurological diseases, which reflects our advances in understanding the pathogenesis of these diseases. Untangling the molecular mechanisms of disease allows monoclonal antibodies to block disease pathways accurately and efficiently with exceptional target specificity, minimizing non-specific effects. On the other hand, accumulating experience shows that monoclonal antibodies may carry class-specific and target-associated risks. 
  • 744
  • 03 Mar 2021
Topic Review
Glial Cells in Ischemia-Reperfusion Injury
Ischemic stroke is the second cause of mortality and the first cause of long-term disability constituting a serious socioeconomic burden worldwide. Approved treatments include thrombectomy and rtPA intravenous administration, which, despite their efficacy in some cases, are not suitable for a great proportion of patients. Glial cell-related therapies are progressively overcoming inefficient neuron-centered approaches in the preclinical phase. Exploiting the ability of microglia to naturally switch between detrimental and protective phenotypes represents a promising therapeutic treatment, in a similar way to what happens with astrocytes. However, the duality present in many of the roles of these cells upon ischemia poses a notorious difficulty in disentangling the precise pathways to target. Still, promoting M2/A2 microglia/astrocyte protective phenotypes and inhibiting M1/A1 neurotoxic profiles is globally rendering promising results in different in vivo models of stroke.
  • 744
  • 08 Sep 2021
Topic Review
Secondary Brain Insults in SE
Status epilepticus (SE) is a major medical condition that is associated with poor outcome in approximately 50% of cases, despite the use of conventional anticonvulsive treatments. The age of the patients, a previous history of epilepsy, SE refractoriness, and a primary cerebral insult as the cause of SE have been identified as independent predictors of poor outcom
  • 742
  • 27 Oct 2020
Topic Review
Tau Aggregates in the Brain
P-tau accumulates with age in a roughly hierarchical manner, but avoids abundance in the neocortex unless co-occurring with amyloid-β. Neurodegenerative tauopathies tend to have p-tau morphologies that differ from aging and Alzheimer’s disease. Tau isoforms (3R vs. 4R) have a tendency to vary with tauopathy phenotype for unknown reasons. Selective vulnerability to p-tau and spatial-temporal disconnect from amyloid-β are evident in aging. P-tau assessment at autopsy involves tissue decomposition, which may skew microanatomical observations toward limited biological meaning. Two major consensus guidelines for interpreting p-tau at autopsy emphasize the challenges of clinicopathologic correlation, and reinforce the observation that regional neurodegeneration is a better correlate of clinical signs than is proteinopathy.
  • 739
  • 22 Dec 2020
Topic Review
Endocannabinoid System
Endocannabinoid System (ECS) is widely distributed in the central nervous system (CNS), constituting a complex signaling system that subserves multiple modes of synaptic transmission modulation. It is expressed at some synapses in all brain regions that are important for the processing of anxiety, fear and stress [1].
  • 730
  • 27 Oct 2020
Topic Review
Brain Neurodegeneration and Cognitive Deficits after Cardiac Arrest
Cardiac arrest occurs as a result of a sudden stop of the heartbeat and its mechanical activity, which causes cessation of systemic circulation and blood flow in the brain, which triggers global brain ischemia. Brain neuropathology after cardiac arrest includes primary ischemic injury and secondary reperfusion injury, which occur sequentially, acutely during cardiac arrest and resuscitation, and chronically in the post-resuscitation stag.
  • 730
  • 29 Feb 2024
Topic Review
Small Fiber Neuropathy in Sarcoidosis
Sarcoidosis (SC) is a granulomatous disease of an unknown origin. The most common SC-related neurological complication is a small fiber neuropathy (SFN) that is often considered to be the result of chronic inflammation and remains significantly understudied. 
  • 729
  • 28 Mar 2022
Topic Review
Nrf2/Keap1/ARE
Alzheimer’s disease (AD) is a progressive neuronal/cognitional dysfunction, leading to disability and death. Despite advances in revealing the pathophysiological mechanisms behind AD, no effective treatment has yet been provided. It urges the need for finding novel multi-target agents in combating the complex dysregulated mechanisms in AD. Amongst the dysregulated pathophysiological pathways in AD, oxidative stress seems to play a critical role in the pathogenesis progression of AD, with a dominant role of nuclear factor erythroid 2-related factor 2 (Nrf2)/Kelch-like ECH-associated protein-1 (Keap1)/antioxidant responsive elements (ARE) pathway. In the present study, a comprehensive review was conducted using the existing electronic databases, including PubMed, Medline, Web of Science, and Scopus, as well as related articles in the field. Nrf2/Keap1/ARE has shown to be the upstream orchestrate of oxidative pathways, which also ameliorates various inflammatory and apoptotic pathways. So, developing multi-target agents with higher efficacy and lower side effects could pave the road in the prevention/management of AD. The plant kingdom is now a great source of natural secondary metabolites in targeting Nrf2/Keap1/ARE. Among natural entities, phenolic compounds, alkaloids, terpene/terpenoids, carotenoids, sulfur-compounds, as well as some other miscellaneous plant-derived compounds have shown promising future accordingly. Prevailing evidence has shown that activating Nrf2/ARE and downstream antioxidant enzymes, as well as inhibiting Keap1 could play hopeful roles in overcoming AD. The current review highlights the neuroprotective effects of plant secondary metabolites through targeting Nrf2/Keap1/ARE and downstream interconnected mediators in combating AD.
  • 725
  • 14 Dec 2020
Topic Review
Cofilin and Neurodegeneration
Cofilin is an actin-binding protein that plays a major role in the regulation of actin dynamics, an essential cellular process. This protein has emerged as a crucial molecule for functions of the nervous system including motility and guidance of the neuronal growth cone, dendritic spine organization, axonal branching, and synaptic signalling. Recently, other important functions in cell biology such as apoptosis or the control of mitochondrial function have been attributed to cofilin. Moreover, novel mechanisms of cofilin function regulation have also been described. The activity of cofilin is controlled by complex regulatory mechanisms, with phosphorylation being the most important, since the addition of a phosphate group to cofilin renders it inactive. Due to its participation in a wide variety of key processes in the cell, cofilin has been related to a great variety of pathologies, among which neurodegenerative diseases have attracted great interest.
  • 725
  • 29 Jul 2021
Topic Review
Chaperone Sigma1R and Antidepressant Effect
The Sigma1R chaperone interacts with cellular mechanisms, which are associated with the formation of a depressive phenotype. Sigma1R is also involved in the pharmacodynamics of antidepressants with various pharmacological targets. As a result of ligand activation, Sigma1R is capable of intracellular translocation from the endoplasmic reticulum (ER) into the region of nuclear and cellular membranes, where it interacts with resident proteins. This unique property of Sigma1R provides regulation of various receptors, ion channels, enzymes, and transcriptional factors. Pharmacological activation of chaperone Sigma1R can be considered a promising strategy to improve and develop approaches for combined, adjuvant pharmacotherapy of depression.
  • 724
  • 09 Oct 2020
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