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Topic Review
Multifaceted Role of Golgi Apparatus
Functioning as the cellular “sorting hub”, the Golgi apparatus is indispensable in protein categorization and adjustments crucial to the dynamic equilibrium of neuronal structure, function, and synaptic adaptability. The Golgi apparatus is not only pivotal in protein categorization and alterations but also stands out as a central orchestrator of neuronal maturation. 
  • 1.3K
  • 26 Sep 2023
Topic Review
Microbiota in Neurodegenerative Disease
Hundreds of billions of commensal microorganisms live in and on human bodies, most of which colonize the gut shortly after birth and stay there for the rest of human lives. In animal models, bidirectional communications between the central nervous system and gut microbiota (Gut–Brain Axis) have been extensively studied, and it is clear that changes in microbiota composition play a vital role in the pathogenesis of various neurodevelopmental and neurodegenerative disorders, such as Autism Spectrum Disorder, Alzheimer’s disease (AD), Parkinson’s disease (PD), Multiple Sclerosis, Amyotrophic Lateral Sclerosis, anxiety, stress, and so on.
  • 1.3K
  • 09 Jun 2022
Topic Review
Innovative Treatments for Glioblastoma
Glioblastoma multiforme (GBM) is a grade IV glioma considered the most fatal cancer of the central nervous system (CNS), with less than a 5% survival rate after five years. The tumor heterogeneity, the high infiltrative behavior of its cells, the low resistance of the brain to ionizing radiations and the blood–brain barrier (BBB) that limits the access of therapeutic drugs to the brain are the main reasons hampering the current standard treatment efficiency.
  • 1.3K
  • 30 Jun 2022
Topic Review
Spinal Cord Injury and Loss of Cortical Inhibition
Amongst the consequences of spinal cord injury (SCI) on the central nervous system, the loss of inhibition is a common finding, albeit not always observed, and it is likely to fluctuate over time. Changes in cortical excitability involve a plethora of mechanisms, which individual effects may combine in complex and variable outcomes on the process of functional and structural recovery. 
  • 1.3K
  • 25 May 2022
Topic Review
Neurotrophins in the Pathogenesis of Alzheimer’s Disease
The involvement of the changed expression/function of neurotrophic factors in the pathogenesis of neurodegenerative diseases, including Alzheimer’s disease (AD), has been suggested. AD is one of the age-related dementias, and is characterized by cognitive impairment with decreased memory function. Developing evidence demonstrates that decreased cell survival, synaptic dysfunction, and reduced neurogenesis are involved in the pathogenesis of AD. On the other hand, it is well known that neurotrophic factors, especially brain-derived neurotrophic factor (BDNF) and its high-affinity receptor TrkB, have multiple roles in the central nervous system (CNS), including neuronal maintenance, synaptic plasticity, and neurogenesis, which are closely linked to learning and memory function. 
  • 1.3K
  • 07 Apr 2023
Topic Review
LOCs/OOCs for Biomedical Applications
Lab-on-a-chip (LOC) and organ-on-a-chip (OOC) devices are highly versatile platforms that enable miniaturization and advanced controlled laboratory functions (i.e., microfluidics, advanced optical or electrical recordings, high-throughput screening). The manufacturing advancements of LOCs/OOCs for biomedical applications and their current limitations are briefly discussed. Multiple studies have exploited the advantages of mimicking organs or tissues on a chip. Among these, we focused our attention on the brain-on-a-chip, blood–brain barrier (BBB)-on-a-chip, and neurovascular unit (NVU)-on-a-chip applications.
  • 1.3K
  • 14 Jul 2021
Topic Review
Calcium Dyshomeostasis in Alzheimer’s Disease
Alzheimer’s disease (AD) is the most common age-related neurodegenerative disorder that is characterized by amyloid β-protein deposition in senile plaques, neurofibrillary tangles consisting of abnormally phosphorylated tau protein, and neuronal loss leading to cognitive decline and dementia. Despite extensive research, the exact mechanisms underlying AD remain unknown and effective treatment is not available. Many hypotheses have been proposed to explain AD pathophysiology; however, there is general consensus that the abnormal aggregation of the amyloid β peptide (Aβ) is the initial event triggering a pathogenic cascade of degenerating events in cholinergic neurons. The dysregulation of calcium homeostasis has been studied considerably to clarify the mechanisms of neurodegeneration induced by Aβ. Intracellular calcium acts as a second messenger and plays a key role in the regulation of neuronal functions, such as neural growth and differentiation, action potential, and synaptic plasticity. The calcium hypothesis of AD posits that activation of the amyloidogenic pathway affects neuronal Ca2+ homeostasis and the mechanisms responsible for learning and memory. Aβ can disrupt Ca2+ signaling through several mechanisms, by increasing the influx of Ca2+ from the extracellular space and by activating its release from intracellular stores. Here, we review the different molecular mechanisms and receptors involved in calcium dysregulation in AD and possible therapeutic strategies for improving the treatment.
  • 1.3K
  • 11 Oct 2021
Topic Review
Piperine in Neurodegenerative and Neurological Diseases
Piperine (PIP) is an active alkaloid of black and long peppers. An increasing amount of evidence is suggesting that PIP and its metabolite’s could be a potential therapeutic to intervene different disease conditions including chronic inflammation, cardiac and hepatic diseases, neurodegenerative diseases, and cancer. In addition, the omnipresence of PIP in food and beverages made this compound an important investigational material. It has now become essential to understand PIP pharmacology and toxicology to determine its merits and demerits, especially its effect on the central nervous system (CNS). Although several earlier reports documented that PIP has poor pharmacokinetic properties, such as absorption, bioavailability, and blood–brain barrier permeability. However, its interaction with metabolic enzyme cytochrome P450 superfamily and competitive hydrophobic interaction at Monoamine oxide B (MAO-B) active site have made PIP both a xenobiotics bioenhancer and a potential MAO-B inhibitor. Moreover, recent advancements in pharmaceutical technology have overcome several of PIP’s limitations, including bioavailability and blood–brain barrier permeability, even at low doses. Contrarily, the structure activity relationship (SAR) study of PIP suggesting that its several metabolites are reactive and plausibly responsible for acute toxicity or have pharmacological potentiality. 
  • 1.3K
  • 07 Feb 2022
Topic Review
The Single Toxin Origin of Alzheimer’s Disease
New data suggest that the aggregation of misfolded native proteins initiates and drives the pathogenic cascade that leads to Alzheimer’s disease (AD) and other age-related neurodegenerative disorders. Researchers propose a unifying single toxin theory of brain neurodegeneration that identifies new targets and approaches to the development of disease-modifying treatments. An extensive body of genetic evidence suggests soluble aggregates of beta-amyloid (Aβ) as the primary neurotoxin in the pathogenesis of AD. New insights from fluid biomarkers, imaging, and clinical studies provide further evidence for the decisive impact of toxic Aβ species in the initiation and progression of AD.
  • 1.3K
  • 21 Mar 2024
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.
  • 1.3K
  • 26 Jul 2021
Topic Review
Emerging Treatments: Targeting Secondary Mechanisms of Neurotrauma
Traumatic central nervous system injury is a leading cause of neurological injury worldwide. While initial neuroresuscitative efforts are focused on ameliorating the effects of primary injury through patient stabilization, secondary injury in neurotrauma is a potential cause of cell death, oxidative stress, and neuroinflammation. These secondary injuries lack defined therapy. The major causes of secondary injury in neurotrauma include endoplasmic reticular stress, mitochondrial dysfunction, and the buildup of reactive oxygen or nitrogenous species. Stress to the endoplasmic reticulum in neurotrauma results in the overactivation of the unfolded protein response with subsequent cell apoptosis. Mitochondrial dysfunction can lead to the release of caspases and the buildup of reactive oxygen species; several characteristics make the central nervous system particularly susceptible to oxidative damage. Together, endoplasmic reticulum, mitochondrial, and oxidative stress can have detrimental consequences, beginning moments and lasting days to months after the primary injury. Understanding these causative pathways has led to the proposal of various potential treatment options.
  • 1.3K
  • 31 May 2022
Topic Review
Extracellular Matrix Regulation in Brain Disease
The extracellular matrix (ECM) surrounds cells in the brain, providing structural and functional support. Emerging studies demonstrate that the ECM plays important roles during development, in the healthy adult brain, and in brain diseases.
  • 1.3K
  • 04 May 2023
Topic Review
Sirt3 and Neurodegenerative Diseases
An NAD+-dependent deacetylase called Sirtuin 3 (Sirt3) is involved in the metabolic processes of the mitochondria, including energy generation, the tricarboxylic acid cycle, and oxidative stress. Sirt3 activation can slow down or prevent mitochondrial dysfunction in response to neurodegenerative disorders, demonstrating a strong neuroprotective impact. The mechanism of Sirt3 in neurodegenerative illnesses has been elucidated over time; it is essential for neuron, astrocyte, and microglial function, and its primary regulatory factors include antiapoptosis, oxidative stress, and the maintenance of metabolic homeostasis. Sirt3 plays a key part in the central nervous system (CNS)  and participates in the regulation of the physiological and pathological functions of various nerve cells. Many of these mechanisms are closely related to neurodegeneration, implying that Sirt3 is a key regulatory molecule in neurodegenerative diseases.
  • 1.3K
  • 15 May 2023
Topic Review
Alcohol Use Disorder and the Brain
Alcohol use disorder (AUD) can be defined as a chronically relapsing disorder characterized by the compulsion to ingest alcohol, the loss of control in limiting alcohol intake despite adverse health, social, and occupational consequences, and the emergence of a negative emotional state that can involve feelings of anxiety, irritability, and dysphoria when access to alcohol is prevented, reflecting a state of motivational withdrawal.
  • 1.3K
  • 31 May 2022
Topic Review
Measles Induced Encephalitis
Encephalitis, a well-known complication of measles, is inflammation of the brain parenchyma which is mostly due to the viral invasion of neurons. It presents with a variety of symptoms ranging from mild to severe depending on the extent of the damaged neurons.
  • 1.3K
  • 28 Nov 2022
Topic Review
Link of Mitochondrial Quality Control and Parkinson’s Disease
Dysfunctional mitochondrial quality control (MQC) is implicated in the pathogenesis of Parkinson’s disease (PD). The improper selection of mitochondria for mitophagy increases reactive oxygen species (ROS) levels and lowers ATP levels. The downstream effects include oxidative damage, failure to maintain proteostasis and ion gradients, and decreased NAD+ and NADPH levels, resulting in insufficient energy metabolism and neurotransmitter synthesis. A ketosis-based metabolic therapy that increases the levels of (R)-3-hydroxybutyrate (BHB) may reverse the dysfunctional MQC by partially replacing glucose as an energy source, by stimulating mitophagy, and by decreasing inflammation. Fasting can potentially raise cytoplasmic NADPH levels by increasing the mitochondrial export and cytoplasmic metabolism of ketone body-derived citrate that increases flux through isocitrate dehydrogenase 1 (IDH1). NADPH is an essential cofactor for nitric oxide synthase, and the nitric oxide synthesized can diffuse into the mitochondrial matrix and react with electron transport chain-synthesized superoxide to form peroxynitrite. Excessive superoxide and peroxynitrite production can cause the opening of the mitochondrial permeability transition pore (mPTP) to depolarize the mitochondria and activate PINK1-dependent mitophagy. Both fasting and exercise increase ketogenesis and increase the cellular NAD+/NADH ratio, both of which are beneficial for neuronal metabolism.
  • 1.3K
  • 31 Aug 2022
Topic Review
Non-Rapid Eye Movement (NREM) Sleep
NREM is important part of the human sleep, and non-pharmacological interventions (acoustic, visual and other stimulations during sleep) are elaborated to modulate it. 
  • 1.3K
  • 20 May 2020
Topic Review
Phyto-Carbazole Alkaloids in Neuroprotection
Plant-derived (phyto) carbazole alkaloids are an important class of compounds, presented in the family of Rutaceae (Genera Murraya, Clausena, Glycosmis, Micromelum and Zanthoxylum). Due to several significant biological activities, such as antitumor, antibacterial, antiviral, antidiabetic, anti-HIV and neuroprotective activities of the parent skeleton (3-methylcarbazole), carbazole alkaloids are recognized as an important class of potential therapeutic agents. Neurodegenerative diseases (NDs) may exhibit a vast range of conditions, affecting neurons primarily and leading ultimately to the progressive losses of normal motor and cognitive functions. The main pathophysiological indicators of NDs comprise increasing atypical protein folding, oxidative stresses, mitochondrial dysfunctions, deranged neurotransmissions and neuronal losses. Phyto-carbazole alkaloids can be investigated for exerting multitarget approaches to ameliorating NDs.
  • 1.3K
  • 19 Apr 2022
Topic Review
Oxidative Pathways in the Pathogenesis of PD
Parkinson’s disease (PD) is a progressive neurodegenerative disorder that arises due to a complex and variable interplay between elements including age, genetic, and environmental risk factors that manifest as the loss of dopaminergic neurons. Contemporary treatments for PD do not prevent or reverse the extent of neurodegeneration that is characteristic of this disorder and accordingly, there is a strong need to develop new approaches which address the underlying disease process and provide benefit to patients with this debilitating disorder. Mitochondrial dysfunction, oxidative damage, and inflammation have been implicated as pathophysiological mechanisms underlying the selective loss of dopaminergic neurons seen in PD.
  • 1.3K
  • 05 Jul 2022
Topic Review
New Frontiers in Peripheral Nerve Regeneration
The peripheral nervous system (PNS) exhibits a limited capacity for functional and morphological repair and regeneration. Peripheral nerve recovery is a multistep process with a complex molecular and cellular regulatory circuitry. Severe injury of peripheral nerves often results in a loss of motor, sensory, and autonomic functions of innervated organs and tissues, therefore calling for novel treatment strategies to ensure effective regeneration.
  • 1.3K
  • 24 Dec 2021
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