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.

Expand All
Topic Review
Molecular Mechanisms of Phenols to Prevent Neurodegeneration
Aging causes changes in brain tissue homeostasis, thus contributing to the development of neurodegenerative disorders. Antioxidant properties of phenolic compounds are of particular interest for neurodegenerative diseases whose psychopathological mechanisms strongly rely on oxidative stress at the brain level. Moreover, phenolic compounds display other advantages such as the permeability of the blood–brain barrier (BBB) and the interesting molecular mechanisms.
  • 106
  • 30 Apr 2024
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.
  • 78
  • 21 Mar 2024
Topic Review
SCD and Genetic Propensity for Dementia beyond Apolipoproteinε4
Subjective cognitive decline (SCD) has been described as a probable early stage of dementia, as it has consistently appeared to precede the onset of objective cognitive impairment. SCD is related to many risk factors, including genetic predisposition for dementia. The Apolipoprotein (APOE) ε4 allele, which has been thoroughly studied, seems to explain genetic risk for SCD only partially.
  • 146
  • 14 Mar 2024
Topic Review
Nitrooxidative Stress and Neuroinflammation Caused by Air Pollutants
Millions of people around the world are exposed to air pollutants, such as particulate matter 2.5 (PM2.5) and ozone (O3). Such exposure usually does not exclude these two types of pollutants and their harmful effects could be additive or synergistic. O3 is a highly oxidizing gas that reacts with the cellular environment just as PM2.5, triggering nitrooxidative damage.
  • 217
  • 13 Mar 2024
Topic Review
Astrocytes and α-Syn in Parkinson’s Disease
The α-syn protein is a 140-amino-acid protein that comprises an N-terminal region that assumes an α-helical secondary structure upon membrane binding, a non-amyloid-component hydrophobic domain that can adopt a β-sheet conformation, promoting protein aggregation in its monomeric form, and a negatively charged C-terminal domain. Astrocytes greatly contribute to neuronal survival through numerous mechanisms, such as the secretion of neurotrophins and antioxidants, the clearance of α-synuclein, glutamate metabolism, fatty acid metabolism, and the transfer of healthy mitochondria to neurons.
  • 91
  • 13 Mar 2024
Topic Review
Cell Autonomous Mechanisms in Astrocytes in Neurodegenerative Diseases
Neurodegenerative disorders like Alzheimer’s disease (AD), Parkinson’s disease (PD), frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) affect millions of people worldwide, and as the average human lifespan increases, similarly grows the number of patients. Cognitive and motoric decline has been explained by the very apparent deterioration of neurons in various regions of the brain and spinal cord. However, more studies show that disease progression is greatly influenced by the vast population of glial cells. Astrocytes are traditionally considered star-shaped cells on which neurons rely heavily for their optimal homeostasis and survival. Increasing amounts of evidence depict how astrocytes lose their supportive functions while simultaneously gaining toxic properties during neurodegeneration. 
  • 101
  • 12 Mar 2024
Topic Review
Pathophysiology-Based Traumatic Brain Injury
Traumatic brain injury (TBI) is a leading cause of disability and death among children and young adults, with an incidence of approximately 1.7 million per year in the USA, resulting in 52,000 deaths. Survivors of the initial impact must still contend with the consequences of trauma, as not all injury occurs at the time of impact. The primary injury results from forces applied to the head and involve direct structural damage to the brain. This triggers a cascade of events leading to neurological damage that evolves secondary injury. Several external brain insults, both intracranial and systemic, may complicate and worsen the secondary injury.
  • 304
  • 07 Mar 2024
Topic Review
Tau Pathology in Alzheimer’s Disease and Down Syndrome
Individuals with Down syndrome (DS) exhibit an almost complete penetrance of Alzheimer’s disease (AD) pathology but are underrepresented in clinical trials for AD. The Tau protein is associated with microtubule function in the neuron and is crucial for normal axonal transport. In several different neurodegenerative disorders, Tau misfolding leads to hyper-phosphorylation of Tau (p-Tau), which may seed pathology to bystander cells and spread.
  • 110
  • 07 Mar 2024
Topic Review
Proteostasis and Proteotoxicity in Network Medicine Era
Neurodegenerative proteinopathies are complex diseases that share some pathogenetic processes. One of these is the failure of the proteostasis network (PN), which includes all components involved in the synthesis, folding, and degradation of proteins, thus leading to the aberrant accumulation of toxic protein aggregates in neurons. The single components that belong to the three main modules of the PN are highly interconnected and can be considered as part of a single giant network.
  • 134
  • 05 Mar 2024
Topic Review
Brain Neurodegeneration and Cognitive Deficits after Cardiac Arrest
Cardiac arrest occurs as a result of a sudden stop of the heartbeat and its mechanical activity, which causes cessation of systemic circulation and blood flow in the brain, which triggers global brain ischemia. Brain neuropathology after cardiac arrest includes primary ischemic injury and secondary reperfusion injury, which occur sequentially, acutely during cardiac arrest and resuscitation, and chronically in the post-resuscitation stag.
  • 261
  • 29 Feb 2024
  • Page
  • of
  • 49