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.
  • 324
  • 29 Sep 2020
Topic Review
Astrocytes
Astrocytes are cerebral cells present in number close to that on neurons (50-60 mld). For decades they were considered only a glue, offering a mechanical and metaboli
  • 344
  • 06 Apr 2021
Topic Review
Atypical Positional Vertigo
Benign paroxysmal positional vertigo is the most frequent cause of vertigo. As its name indicates, it is characterized by vertigo episodes of sudden onset and end, triggered by changes in head’s position with regard to gravity. It is located in the labyrinth, and its cause is mechanical. However, this is an etiologic diagnosis, reached after questioning and examining the patient. Based on what patients report, the duration of symptoms lasts seconds; however, many overestimate the duration of the vertiginous sensation. The trigger effect of positional changes is a key issue to be addressed. A great variability of autonomic symptoms, including nausea and vomiting, can accompany BPPV. Gait instability, headache, and additional neurologic complaints are potential red flags in the differential diagnosis. With a defined position trigger effect, it is the neurologist’s job to perform an examination to confirm the diagnosis of paroxysmal positional vertigo (PPV), and by virtue of the vertigo duration and nystagmus characteristics, to determine lesion localization (peripheral versus central) and to design a management plan.
  • 131
  • 26 May 2022
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.
  • 239
  • 10 Mar 2021
Topic Review
Autophagy and Alzheimer’s Disease
Alzheimer’s disease (AD) is characterized by the formation of intracellular aggregate composed of heavily phosphorylated tau protein and extracellular deposit of amyloid-β (Aβ) plaques derived from proteolysis cleavage of amyloid precursor protein (APP). Autophagy refers to the lysosomal-mediated degradation of cytoplasmic constituents, which plays a critical role in maintaining cellular homeostasis. Importantly, recent studies reported that dysregulation of autophagy is associated in the pathogenesis of AD, and therefore, autophagy modulation has gained attention as a promising approach to treat AD pathogenesis. In AD, both the maturation of autolysosomes and its retrograde transports have been obstructed, which causes the accumulation of autophagic vacuoles and eventually leads to degenerating and dystrophic neurites function. However, the mechanism of autophagy modulation in APP processing and its pathogenesis have not yet been fully elucidated in AD. In the early stage of AD, APP processing and Aβ accumulation-mediated autophagy facilitate the removal of toxic protein aggregates via mTOR-dependent and -independent pathways. In addition, a number of autophagy-related genes (Atg) and APP are thought to influence the development of AD, providing a bidirectional link between autophagy and AD pathology.
  • 320
  • 28 Sep 2021
Topic Review
Autophagy and Neurodegenerative Diseases
The word autophagy was introduced in late 1963 by the biochemist Christian de Duve [18] and defines a self-degradative cellular pathway whose intent is to degrade and recycle cellular contents. Autophagy exists in three forms that are classified according to their mechanisms and cellular functions: macroautophagy, microautophagy, and chaperone-mediated autophagy (CMA). During microautophagy, the cytosolic material is wrapped and transported directly into the lumen of lysosomes. The main function of microautophagy (mA) is to control cell survival and organellar turnover upon nitrogen restriction. CMA has an important role in protein quality control (QC) and is responsible for degrading a specific subset of oxidized and damaged proteins. The selectivity of CMA is conferred by the existence of a specific pentapeptide motif (KFERQ), which is present in the amino acid sequences of all CMA substrates. Undoubtedly, the best-characterized and most prevalent form of autophagy in mammalian cells is macroautophagy (hereafter referred to as autophagy). Autophagy is responsible to capture a wide group of intracellular components, ranging from low-dimensional biological macromolecules to whole organelles, and bring them to the lysosomal compartment. Its physiological value rests on two main activities. On the one hand, autophagy acts as a QC mechanism that reshapes the cell, ensuring the removal of damaged proteins and organelles [27]. Selective forms of autophagy can specifically target mitochondria (mitophagy), the endoplasmic reticulum (ER; reticulophagy), peroxisomes (pexophagy), and lipid droplets (lipophagy).
  • 190
  • 16 Apr 2021
Topic Review
Autophagy in Alzheimer’s Disease
Aging and the emergence of age-associated illnesses are one of the major challenges of our present society. Alzheimer’s disease (AD) is closely associated with aging and is defined by increasing memory loss and severe dementia. Currently, there are no therapy options available that halt AD progression. 
  • 218
  • 08 Jan 2021
Topic Review
Axonal Regeneration in CNS Damage
Central nervous system (CNS) damage caused by traumatic injuries, iatrogenicity due to surgical interventions, stroke and neurodegenerative diseases is one of the most prevalent reasons for physical disability worldwide. During development, axons must elongate from the neuronal cell body to contact their precise target cell and establish functional connections. However, the capacity of the adult nervous system to restore its functionality after injury is limited. Given the inefficacy of the nervous system to heal and regenerate after damage, new therapies are under investigation to enhance axonal regeneration. Axon guidance cues and receptors, as well as the molecular machinery activated after nervous system damage, are organized into lipid raft microdomains, a term typically used to describe nanoscale membrane domains enriched in cholesterol and glycosphingolipids that act as signaling platforms for certain transmembrane proteins.
  • 133
  • 25 May 2021
Topic Review Peer Reviewed
Benefits of Table Tennis for Brain Health Maintenance and Prevention of Dementia
Table tennis is an extremely popular sport throughout the world as it requires no expensive equipment, specialized amenities, or physical contact among players, and the pace of play can be adapted to allow participation by players of all skill levels, ages, and abilities. It is an aerobic-dominant sport driven primarily by the phosphagen system because rallies are relatively brief (several seconds) and separated by longer rest periods. Several studies have shown that physical interventions including table tennis can help prevent cognitive decline and dementia. Accordingly, the present paper provides an overview of the basic physical and cognitive demands of table tennis, reviews previous studies reporting improvements in physical and brain health across different non-clinical and clinical populations, and critically evaluates the usefulness of table tennis intervention for the prevention of cognitive decline and dementia. This review suggests that table tennis intervention could be a powerful strategy to prevent cognitive decline and dementia in the elderly. 
  • 611
  • 26 Sep 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. 
  • 23
  • 21 Oct 2022
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