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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.
  • 780
  • 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).
  • 489
  • 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. 
  • 493
  • 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.
  • 370
  • 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. 
  • 2.3K
  • 26 Sep 2022
Topic Review
Blood-Based Biomarkers in Chronic Traumatic Encephalopathy Diagnosis
Chronic Traumatic Encephalopathy (CTE) is a neurodegenerative disease consistently associated with repetitive traumatic brain injuries (TBIs), which makes multiple professions, such as contact sports athletes and the military, especially susceptible to its onset. There are currently no approved biomarkers to diagnose CTE, thus it can only be confirmed through a post-mortem brain autopsy. Several imaging and cerebrospinal fluid biomarkers have shown promise in the diagnosis. However, blood-based biomarkers can be more easily obtained and quantified, increasing their clinical feasibility and potential for prophylactic use. 
  • 799
  • 29 Aug 2023
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. 
  • 380
  • 21 Oct 2022
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.
  • 610
  • 31 Jan 2021
Topic Review
Botulinum Toxin Type A for Restless Legs Syndrome
Restless legs syndrome (RLS) is a sleep-related movement disorder characterized by an unpleasant urge to move the lower limbs. The prevalence of RLS varies by region, ethnicity, sex, and age, ranging from 5–15% . Its pathophysiology remains unclear. Criteria for the diagnosis of RLS include the International Restless Legs Syndrome Study Group (IRLSSG) and International Classification of Sleep Disorders, Third Edition (ICSD-3). The ICSD-3 criteria require distress and associated sleep disturbance, which is different from the IRLSSG consensus [2]. As for the measurement of disease severity for RLS, the IRLSSG rating scale (IRLS) was proposed. It assesses a range of RLS related symptoms and their impact on patients’ mood and daily life, and it has been proved reliable, valid, and responsive in clinical trials.
  • 363
  • 18 Nov 2021
Topic Review
Botulinumtoxin A for Post-herpetic neuralgia
Post-herpetic neuralgia (PHN) is a very painful neuropathic condition, which occurs after nerve injury (e.g., demyelination, loss of axons, small-fiber-degeneration, reorganization in the dorsal horn of the spinal cord, and neuroplastic central changes) due to herpes-zoster-virus infection and is defined as a local neuropathic pain lasting for more than three months following the initial acute zoster infection.  Adjunctive local BoNT A injection is a promising option for severe PHN, as a safe and effective therapy in long-term management for chronic neuropathic pain.
  • 429
  • 16 Jan 2022
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