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
Mental States and Molecular Biology
Today, it is possible to investigate the biological paths and mechanisms that link mental life to biological life. Emotions, feelings, desires, and cognitions influence biological systems. In recent decades, psychoneuroendocrinoimmunology research has highlighted the routes linking the psyche–brain–immune systems. Recently, epigenetics research has shown the molecular mechanisms by which stress and mental states modulate the information contained in the genome.
  • 594
  • 09 May 2022
Topic Review
Effect of Physical Exercise in Alzheimer’s Disease Patients
Physical exercise (PE) can be a non-pharmacological intervention in delaying cognitive decline in patients with Alzheimer’s disease (AD) not only by improving cardiovascular fitness but also by attenuating neuroinflammation. Animal studies consistently report that PE improves cardiovascular fitness and attenuates AD-promoting processing of amyloid precursor protein and neuroinflammation, facilitates brain clearance of toxic amyloid β peptides and oligomers and promotes brain connectivity and nerve cell viability. Further studies in human are necessary to develop optimal, personalised protocols to take full advantage of the beneficial effects of PE that promote cardiovascular fitness, attenuate systemic inflammation, stimulate brain amyloid β peptides brain catabolism, delay immunescence and support brain clearance of amyloid β peptides and their catabolism in peripheral organs.
  • 459
  • 06 May 2022
Topic Review
Neuroinflammation in Parkinson’s Disease
Parkinson’s disease (PD) is a common neurodegenerative disease characterized by the loss of dopaminergic (DAergic) neurons in the substantia nigra pars compacta (SNpc). Its main symptoms include resting tremors, rigidity, shuffling gait, and bradykinesia. Genome-wide association studies have identified many genetic variants associated with PD. Studies of animal models, neuroimages, and postmortem pathology have also provided substantial insights into the involvement of neuroinflammation in PD pathogenesis, and indicate that cytokine-induced inflammatory responses may play a vital role.
  • 416
  • 05 May 2022
Topic Review
Diffuse Axonal Injury
Diffuse axonal injuries (DAI) are the result of strong rotational and translational forces on the brain parenchyma, leading to cerebral oedema and neuronal death. DAI is typically characterized by coma without focal lesions at presentation and is defined by localized axonal damage in multiple regions of the brain parenchyma, often causing impairment of cognitive and neuro-vegetative function.
  • 498
  • 05 May 2022
Topic Review
Dictyostelium discoideum
Dictyostelium discoideum has provided a useful, simple model to aid in unraveling the complex pathological characteristics of neurological disorders including Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, neuronal ceroid lipofuscinoses and lissencephaly. 
  • 588
  • 06 May 2022
Topic Review
Experimental Models for Neonatal Hypoxic-Ischemic Encephalopathy
Representing an important cause of long–term disability, term neonatal hypoxic-ischemic encephalopathy (HIE) urgently needs further research aimed at repurposing existing drug as well as developing new therapeutics. Since various experimental in vitro and in vivo models of HIE have been developed with distinct characteristics, it becomes important to select the appropriate preclinical screening cascade for testing the efficacy of novel pharmacological treatments.
  • 493
  • 05 May 2022
Topic Review
Alzheimer’s Disease and Tau Self-Assembly
Alzheimer’s disease (AD) is a multifactorial neurodegenerative disease characterized by progressive cognitive impairment, apathy, and neuropsychiatric disorders. Two main pathological hallmarks have been described: neurofibrillary tangles, consisting of tau oligomers (hyperphosphorylated tau) and Aβ plaques. The influence of protein kinases and phosphatases on the hyperphosphorylation of tau is already known. Hyperphosphorylated tau undergoes conformational changes that promote its self-assembly. 
  • 704
  • 28 Apr 2022
Topic Review
Toxin-Based Models of Parkinson’s Disease
Different neurotoxins have been shown to cause DAergic neuron degeneration with a high degree of selectivity. Some utilize the dopamine transporter to enter the neurons, others are lipophilic agents or neurotransmitter receptors' agonists that, directly or indirectly, ultimately impair the mitochondrial respiratory chain. Taking advantage of these properties, several molecules have been extensively used to obtain PD experimental models. These include 6-OHDA, MPTP (MPP+), the pesticides rotenone and paraquat, and the non-protein aminoacid L-BMAA.
  • 646
  • 29 Apr 2022
Topic Review
Biomarker of Neuroinflammation in Parkinson’s Disease
Parkinson's disease is caused by an abnormal accumulation of alfa-synuclein in dopaminergic neurons of the substantial nigra, which subsequently causes motor symptoms. Neuroinflammation plays a vital role in the pathogenesis of neurodegeneration in PD. This neuroinflammatory neurodegeneration involves the activation of microglia, upregulation of proinflammatory factors, and gut microbiota.
  • 431
  • 29 Apr 2022
Topic Review
Nucleolar and Ribosomal Dysfunction
Ageing is a complex and unavoidable process that can be defined as the functional decline after a period of maturity. In this respect, maturity is understood as the endpoint of development and the condition of maximal functional performance capability.  The nucleolus organizes around the sites of transcription by RNA polymerase I (RNA Pol I). rDNA transcription by this enzyme is the key step of ribosome biogenesis and most of the assembly and maturation processes of the ribosome occur co-transcriptionally. Therefore, disturbances in rRNA transcription and processing translate to ribosomal malfunction. Nucleolar malfunction has recently been described in the classical progeria of childhood, Hutchinson–Gilford syndrome (HGPS), which is characterized by severe signs of premature aging, including atherosclerosis, alopecia, and osteoporosis. A deregulated ribosomal biogenesis with enlarged nucleoli is not only characteristic for HGPS patients, but it is also found in the fibroblasts of “normal” aging individuals. Cockayne syndrome (CS) is also characterized by signs of premature aging, including the loss of subcutaneous fat, alopecia, and cataracts. It has been shown that all genes in which a mutation causes CS, are involved in rDNA transcription by RNA Pol I. 
  • 584
  • 27 Apr 2022
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