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Topic Review
Neurocognitive Psychiatric and Neuropsychological Alterations in Parkinson’s Disease
The main histopathological hallmarks of Parkinson’s disease (PD) are the degeneration of the dopaminergic neurons of the substantia nigra pars compacta and the loss of neuromelanin as a consequence of decreased dopamine synthesis. The destruction of the striatal dopaminergic pathway and blocking of striatal dopamine receptors cause motor deficits in humans and experimental animal models induced by some environmental agents. In addition, neuropsychiatric symptoms such as mood and anxiety disorders, hallucinations, psychosis, cognitive impairment, and dementia are common in PD. These alterations may precede the appearance of motor symptoms and are correlated with neurochemical and structural changes in the brain. 
  • 1.3K
  • 23 Mar 2023
Topic Review
Psychiatric Disorders
Psychiatric disorders refer to the behavior or psychological pattern that can lead to significant distress or functional impairment.
  • 1.2K
  • 01 Feb 2021
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.
  • 1.2K
  • 29 Jul 2021
Topic Review
Chronic Dexamethasone Treatment
Neuroinflammation has been correlated with the progress of neurodegeneration in many neuropathologies. Although glial cells have traditionally been considered to be protective, the concept of them as neurotoxic cells has recently emerged. Thus, a major unsolved question is the exact role of astroglia and microglia in neurodegenerative disorders. On the other hand, it is well known that glucocorticoids are the first choice to regulate inflammation and, consequently, neuroglial inflammatory activity. The objective of this study was to determine how chronic dexamethasone treatment influences the host immune response and to characterize the beneficial or detrimental role of glial cells. To date, this has not been examined using a natural neurodegenerative model of scrapie. With this aim, immunohistochemical expression of glial markers, prion protein accumulation, histopathological lesions and clinical evolution were compared with those in a control group. Although impact of dexamethasone administration on neuropathological lesions was not demonstrated and treatment did not seem to be clinically relevant to disease progress when clinical signs had already begun, the evident extension of survival in one case was hopeful. The findings presented in this study support a potential failure of astrocytes and a stimulation of phagocytosis of PrPsc deposits by microglia. Thus, it is evidenced here how the complex interaction between glial populations failed to compensate for brain damage in natural conditions, emphasizing the need for using natural models. Additionally, the data showed that modulation of neuroinflammation by anti-inflammatory drugs might become a research focus as a potential therapeutic target for prion diseases, similar to that considered previously for other neurodegenerative disorders classified as prion-like diseases.
  • 1.2K
  • 28 Oct 2020
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. 
  • 1.2K
  • 03 Feb 2023
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.
  • 1.2K
  • 26 Jul 2021
Topic Review
Leptin Cellular Signaling in Brain
The triad of obesity, metabolic syndrome (MetS), Type 2 diabetes mellitus (T2DM) and advancing age are currently global societal problems that are expected to grow over the coming decades. This triad is associated with multiple end-organ complications of diabetic vasculopathy (maco-microvessel disease), neuropathy, retinopathy, nephropathy, cardiomyopathy, cognopathy encephalopathy and/or late-onset Alzheimer’s disease. 
  • 1.2K
  • 01 Jun 2021
Topic Review
Mesoporous Silica Nanoparticles for Treatment of Alzheimer’s Disease
Globally, many individuals struggle with Alzheimer’s disease (AD), an unrelenting and incapacitating neurodegenerative condition. Despite notable research endeavors, effective remedies for AD remain constrained, prompting the exploration of innovative therapeutic avenues. Within this context, silica-based nanoplatforms have emerged with pronounced potential due to their unique attributes like expansive surface area, customizable pore dimensions, and compatibility with living systems. These nanoplatforms hold promise as prospective interventions for AD.
  • 1.2K
  • 01 Dec 2023
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.
  • 1.2K
  • 08 Feb 2022
Topic Review
Botulinum Toxin in Chronic Migraine Treatment
Primary headaches are a large group of diseases where the headache is not a symptom of another known disease. Tension-type headache affects approximately 80% of the general population, and the prevalence of migraine is estimated at 10–12%. Clinical data and experience to date have demonstrated that botulinum toxin may be an effective prophylactic treatment for chronic headache types. It has been used in neurology for the treatment of dystonia and blepharospasm. Now it has been approved to treat chronic migraine and has been shown to confer significant benefit in refractory cases.  Botulinum toxin is effective in pain control through its interaction with the SNARE complex, which inhibits the release of neurotransmitters, such as glutamate, substance P and calcitonin gene-related peptide. OnabotulinumtoxinA is effective not only in headache frequency and pain intensity but in other parameters, including quality of life. 
  • 1.2K
  • 21 Oct 2022
Topic Review
Pharmacological and Non-Pharmacological Treatments for Depression in PD
Depression represents one of the most common non-motor disorders in Parkinson’s disease (PD) and it has been related to worse life quality, higher levels of disability, and cognitive impairment, thereby majorly affecting not only the patients but also their caregivers. Available pharmacological therapeutic options for depression in PD mainly include selective serotonin reuptake inhibitors, serotonin and norepinephrine reuptake inhibitors, and tricyclic antidepressants; meanwhile, agents acting on dopaminergic pathways used for motor symptoms, such as levodopa, dopaminergic agonists, and monoamine oxidase B (MAO-B) inhibitors, may also provide beneficial antidepressant effects. There is a growing interest in non-pharmacological interventions, including cognitive behavioral therapy; physical exercise, including dance and mind–body exercises, such as yoga, tai chi, and qigong; acupuncture; therapeutic massage; music therapy; active therapy; repetitive transcranial magnetic stimulation (rTMS); and electroconvulsive therapy (ECT) for refractory cases.
  • 1.2K
  • 01 Sep 2023
Topic Review
Degenerative Cervical Myelopathy
Degenerative cervical myelopathy (DCM), earlier referred to as cervical spondylotic myelopathy (CSM), is the most common and serious neurological disorder in the elderly population caused by chronic progressive compression or irritation of the spinal cord in the neck. The clinical features of DCM include localised neck pain and functional impairment of motor function in the arms, fingers and hands. If left untreated, this can lead to significant and permanent nerve damage including paralysis and death.
  • 1.2K
  • 11 May 2021
Topic Review
Synaptic Disruption by Soluble Oligomers in Neurodegenerative Diseases
Neurodegenerative diseases are the result of progressive dysfunction of the neuronal activity and subsequent neuronal death. Currently, the most prevalent neurodegenerative diseases are by far Alzheimer’s (AD) and Parkinson’s (PD) disease, affecting millions of people worldwide. Although amyloid plaques and neurofibrillary tangles are the neuropathological hallmarks for AD and Lewy bodies (LB) are the hallmark for PD, current evidence strongly suggests that oligomers seeding the neuropathological hallmarks are more toxic and disease-relevant in both pathologies. The presence of small soluble oligomers is the common bond between AD and PD: amyloid β oligomers (AβOs) and Tau oligomers (TauOs) in AD and α-synuclein oligomers (αSynOs) in PD. Such oligomers appear to be particularly increased during the early pathological stages, targeting synapses at vulnerable brain regions leading to synaptic plasticity disruption, synapse loss, inflammation, excitation to inhibition imbalance and cognitive impairment. Absence of TauOs at synapses in individuals with strong AD disease pathology but preserved cognition suggests that mechanisms of resilience may be dependent on the interactions between soluble oligomers and their synaptic targets.
  • 1.2K
  • 31 Aug 2022
Topic Review
HMGB1-Mediated Neuroinflammatory Responses
Brain injuries are devastating conditions, representing a global cause of mortality and morbidity, with no effective treatment to date. Increased evidence supports the role of neuroinflammation in driving several forms of brain injuries. High mobility group box 1 (HMGB1) protein is a pro-inflammatory-like cytokine with an initiator role in neuroinflammation that has been implicated in Traumatic brain injury (TBI) as well as in early brain injury (EBI) after subarachnoid hemorrhage (SAH). Herein, we discuss the implication of HMGB1-induced neuroinflammatory responses in these brain injuries, mediated through binding to the receptor for advanced glycation end products (RAGE), toll-like receptor4 (TLR4) and other inflammatory mediators. Moreover, we provide evidence on the biomarker potential of HMGB1 and the significance of its nucleocytoplasmic translocation during brain injuries along with the promising neuroprotective effects observed upon HMGB1 inhibition/neutralization in TBI and EBI induced by SAH. Overall, this review addresses the current advances on neuroinflammation driven by HMGB1 in brain injuries indicating a future treatment opportunity that may overcome current therapeutic gaps.
  • 1.2K
  • 23 Jul 2020
Topic Review
Autism Spectrum Disorder (ASD)
Autism Spectrum Disorder etiopathogenesis is still unclear, no effective preventive and treatment measures have been identified.  Research has focused on the potential role of neuroinflammation and kynurenine pathway. Pre-natal or neonatal infections would induce microglial activation, with secondary consequences on behavior, cognition and neurotransmitter networks. Peripherally higher levels of pro-inflammatory cytokines,  and anti-brain antibodies have been identified. Increased frequency of autoimmune diseases, allergies, and recurring infections have been demonstrated both in autistic patients and in their relatives. Genetic studies, also, have identified some important polymorphisms in chromosome loci related to human leukocyte antigen (HLA) system. The persistence of immune-inflammatory deregulation, would lead to mitochondrial dysfunction and oxidative stress, creating a self-sustaining cytotoxic loop. Chronic inflammation actives kynurenine pathway with increase in neurotoxic metabolites and excitotoxicity, causing long-term changes in glutamatergic function, trophic support and synaptic function. Furthermore, overactivation of kynurenines branch, induces depletion of melatonin and serotonin, with  ASD symptoms worsening.According to those findings, in subjects genetically predisposed an aberrant neurodevelopment derives by a complex interplay between inflammatory process, mitochondrial dysfunction, oxidative stress, kynurenine pathway overactivation.To validate the previous hypothesis a new translational research approach is necessary.
  • 1.2K
  • 10 Mar 2021
Topic Review
S100B for Management of Mild Traumatic Brain Injury
(S100 calcium-binding protein B) S100B protein has emerged as the most widely studied and used biomarker for clinical decision making in patients with mTBI. In addition to its use as a diagnostic biomarker, S100B plays an active role in the molecular pathogenic processes accompanying acute brain injury.
  • 1.2K
  • 12 Apr 2023
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.
  • 1.1K
  • 29 Oct 2020
Topic Review
Nanomedicine for Stroke Diagnosis
Ischemic stroke, caused by the interruption of blood flow to the brain and subsequent neuronal death, represents one of the main causes of disability in developed countries. Therapeutic methods such as recanalization approaches, neuroprotective drugs, or recovery strategies have been widely developed to improve the patient’s outcome; however, important limitations such as a narrow therapeutic window, the ability to reach brain targets, or drug side effects constitute some of the main aspects that limit the clinical applicability of the current treatments. Nanotechnology has emerged as a promising tool to overcome many of these drug limitations and improve the efficacy of treatments for neurological diseases such as stroke. 
  • 1.1K
  • 04 Jun 2021
Topic Review
Astrocyte–Neuron Crosstalk
Astrocyte-neuron crosstalk is a phenomenon in which both of those cell types depend on each other and support their development, genes expression, metabolism, excitability and plasticity. Astrocyte–neuron crosstalk incontrovertibly plays a crucial role in shaping neuronal metabolism. It has been shown that it substantially affects the expression of basal metabolic enzymes in both types of cells, by essentially unknown factor(s) which are released to extracellular space directly and using extracellular vesicles-packed molecules and by cell-to-cell contacts. Additionally, astrocytes support neurons with lactate, which (when secreted during enhanced neuronal activity events) stimulates a formation and maintenece of long-term plastycity phenomena in neurons.
  • 1.1K
  • 29 Sep 2020
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.
  • 1.1K
  • 22 Apr 2021
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