Summary

Neurodegeneration refers to the progressive loss of neuron structure or function, which may eventually lead to cell death. Many neurodegenerative diseases, such as amyotrophic lateral sclerosis, multiple sclerosis, Parkinson's disease, Alzheimer's disease, Huntington's disease and prion disease, are the results of neurodegenerative processes. Neurodegeneration can be found in many different levels of neuronal circuits in the brain, from molecules to systems. Since there is no known method to reverse the progressive degeneration of neurons, these diseases are considered incurable. Biomedical research has revealed many similarities between these diseases at the subcellular level, including atypical protein assembly (such as protein diseases) and induction of cell death. These similarities indicate that progress in the treatment of one neurodegenerative disease may also improve other diseases. This collection of entries aims to collect various medical research results related to neurodegeneration. We invite researchers to share their new results and ideas related to neurodegeneration.

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Entries
Topic Review
Microglia Depletion in Spinal Cord Injury Treatment
Microglia, as the resident immune cells and first responder to neurological insults, play an extremely important role in the pathophysiological process of spinal cord injury. On the one hand, microglia respond rapidly and gather around the lesion in the early stage of injury to exert a protective role, but with the continuous stimulation of the injury, the excessive activated microglia secrete a large number of harmful substances, aggravate the injury of spinal cord tissue, and affect functional recovery. The effects of microglia depletion on the repair of spinal cord injury remain unclear, and there is no uniformly accepted paradigm for the removal methods and timing of microglia depletion, but different microglia depletion strategies greatly affect the outcomes after spinal cord injury.
  • 402
  • 15 Jun 2022
Topic Review
Neuroprotective Agents from Syzygium from Alzheimer’s Perspective
Alzheimer’s disease (AD) is the most prevalent type of dementia worldwide, constituting 70–80% of cases, primarily among the elderly. This irreversible neurodegenerative disorder progressively impairs memory and other cognitive functions. The molecular mechanisms of Syzygium species in neuroprotection include the inhibition of acetylcholinesterase (AChE) to correct cholinergic transmission, suppression of pro-inflammatory mediators, oxidative stress markers, reactive immediate species (RIS) production, enhancement of antioxidant enzymes, the restoration of brain ions homeostasis, the inhibition of microglial invasion, the modulation of ß-cell insulin release, the enhancement of lipid accumulation, glucose uptake, and adiponectin secretion via the activation of the insulin signaling pathway. Additional efforts are warranted to explore less studied species, including the Australian and Western Syzygium species. The effectiveness of the Syzygium genus in neuroprotective responses is markedly established, but further compound isolation, in silico, and clinical studies are demanded. 
  • 602
  • 14 Jun 2022
Topic Review
The Microglia in Brain Ischemia-Reperfusion Injury
Microglia represent 10–15% of the total cells in the brain. These cells are considered as the resident macrophages and the first defense line in the central nervous system (CNS) against pathogens. Microglial activation is one of the earliest events after brain ischemia. 
  • 1.2K
  • 20 Jun 2022
Topic Review
Nuclear Factor-E2-Related Factor 2 in Neurodegenerative Disorders
Nuclear factor-E2-related factor 2 (Nrf2) is a short-lived protein that works as a transcription factor and is related to the expression of many cytoprotective genes involved in xenobiotic metabolism and antioxidant responses. Nrf2 is a key regulator of OS defense and research supports a protective and defending role of Nrf2 against neurodegenerative conditions.
  • 551
  • 10 Jun 2022
Topic Review
CXCL1 in Noncancerous Diseases of the Nervous System
Chemokines are chemotactic cytokines, whose most important function is the chemoattraction of immune cells. CXC motif chemokine ligand 1 (CXCL1), a CXC chemokine, is also known as growth-regulated (or -related) oncogene-α (Gro-α) and melanoma growth-stimulatory activity (MGSA). The role CXCL1 plays in the physiology of the nervous system is described. 
  • 704
  • 10 Jun 2022
Topic Review
Role of Antimicrobial Peptides in Alzheimer's Disease
Alzheimer’s disease (AD) represents the most frequent type of dementia in elderly people. There are two major forms of the disease: sporadic (SAD) - whose causes are not completely understood - and familial (FAD) - with clear autosomal dominant inheritance. The two main hallmarks of AD are extracellular deposits of amyloid-beta (Aβ) peptide and intracellular deposits of the hyperphosphorylated form of the tau protein (P-tau). An ever-growing body of research supports the infectious hypothesis of sporadic forms of AD.
  • 486
  • 10 Jun 2022
Topic Review
Neuroinflammation in Friedreich’s Ataxia
Friedreich’s ataxia (FRDA) is a rare genetic disorder caused by mutations in the gene frataxin, encoding for a mitochondrial protein involved in iron handling and in the biogenesis of iron−sulphur clusters, and leading to progressive nervous system damage.
  • 794
  • 10 Jun 2022
Topic Review
NEDD4 E3 Ubiquitin–Protein Ligases in Parkinson’s Disease
Parkinson’s disease (PD) is a debilitating neurodegenerative disease that causes a great clinical burden. However, its exact molecular pathologies are not fully understood. Whilst there are a number of avenues for research into slowing, halting, or reversing PD, one central idea is to enhance the clearance of the proposed aetiological protein, oligomeric α-synuclein. Oligomeric α-synuclein is the main constituent protein in Lewy bodies and neurites and is considered neurotoxic. Multiple E3 ubiquitin-protein ligases, including the NEDD4 (neural precursor cell expressed developmentally downregulated protein 4) family, parkin, SIAH (mammalian homologues of Drosophila seven in absentia), CHIP (carboxy-terminus of Hsc70 interacting protein), and SCFFXBL5 SCF ubiquitin ligase assembled by the S-phase kinase-associated protein (SKP1), cullin-1 (Cul1), a zinc-binding RING finger protein, and the F-box domain/Leucine-rich repeat protein 5-containing protein FBXL5), have been shown to be able to ubiquitinate α-synuclein, influencing its subsequent degradation via the proteasome or lysosome. Some members of the NEDD4 family of ligases are thought to crosstalk even with PD-related genes and proteins found to be mutated in familial forms of PD. Mutations in NEDD4 family genes have not been observed in PD patients, most likely because of their essential survival function during development. It has been thought that NEDD4 ligases may be viable therapeutic targets in PD. NEDD4 family members could clear toxic proteins, enhancing cell survival and slowing disease progression, or might diminish beneficial proteins, reducing cell survival and accelerating disease progression. 
  • 522
  • 10 Jun 2022
Topic Review
α-Synuclein Phosphorylation and Its Kinases
α-Synuclein is a protein with a molecular weight of 14.5 kDa and consists of 140 amino acids encoded by the SNCA gene. Missense mutations and gene duplications in the SNCA gene cause hereditary Parkinson’s disease. Highly phosphorylated and abnormally aggregated α-synuclein is a major component of Lewy bodies found in neuronal cells of patients with sporadic Parkinson’s disease, dementia with Lewy bodies, and glial cytoplasmic inclusion bodies in oligodendrocytes with multiple system atrophy. Aggregated α-synuclein is cytotoxic and plays a central role in the pathogenesis of the above-mentioned synucleinopathies. In a healthy brain, most α-synuclein is unphosphorylated; however, more than 90% of abnormally aggregated α-synuclein in Lewy bodies of patients with Parkinson’s disease is phosphorylated at Ser129, which is presumed to be of pathological significance. Several kinases catalyze Ser129 phosphorylation, but the role of phosphorylation enzymes in disease pathogenesis and their relationship to cellular toxicity from phosphorylation are not fully understood in α-synucleinopathy. G-protein-coupled receptor kinases, casein kinase II, and polo-like kinase possess the ability to phosphorylate α-synuclein protein. On this point, inhibition of these kinases is able to prevent α-synuclein phosphorylation, which indicates the potential therapeutic targets and availability of drug development for α-synucleinopathies. α-Synuclein phosphorylation can clinically be an accompanying event in the brains of patients with Parkinson’s disease rather than the critical factor for α-synuclein aggregation and toxicity. Nevertheless, increasing phosphorylated α-synuclein and the accumulation with disease progression is useful as a therapeutic target and biomarker.
  • 534
  • 08 Jun 2022
Topic Review
The Microbial Hypothesis of Alzheimer’s Disease
The potential contribution of pathogenic microbes to dementia-inducing disease is a subject of considerable importance. Alzheimer’s disease (AD) is a neurocognitive disease that slowly destroys brain function, leading to cognitive decline and behavioral and psychiatric disorders. The histopathology of AD is associated with neuronal loss and progressive synaptic dysfunction, accompanied by the deposition of amyloid-β (Aβ) peptide in the form of parenchymal plaques and abnormal aggregated tau protein in the form of neurofibrillary tangles. The AD pathogen hypothesis states that pathogens and microbes act as triggers, interacting with genetic factors to initiate the accumulation of Aβ, hyperphosphorylated tau protein (p-tau), and inflammation in the brain. Evidence indicates that Borrelia sp., HSV-1, VZV (HHV-2), HHV-6/7, oral pathogens, Chlamydophila pneumoniae, and Candida albicans can infect the central nervous system (CNS), evade the immune system, and consequently prevail in the AD brain.
  • 887
  • 06 Jun 2022
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