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.

Expand All
Entries
Topic Review
Oligodendrocytes and Vitamin D Neuroprotection in Multiple Sclerosis
Multiple sclerosis (MS) is a complex neurological condition that involves both inflammatory demyelinating and neurodegenerative components. MS research and treatments have traditionally focused on immunomodulation, with less investigation of neuroprotection, and this holds true for the role of vitamin D in MS. Vitamin D plays an anti-inflammatory role in modulating the immune system in MS. More recently, researchers have begun investigating the potential neuroprotective role of vitamin D in MS, which may be important in remyelination and/or the prevention of demyelination. There is a growing body of research uncovering mechanistic role of vitamin D-mediated neuroprotection, including: enhancing oligodendrocyte lineage differentiation, enhancing neurotrophin expression, attenuating aberrant microglial and reactive astrocyte activation, stabilizing the BBB, and reducing oxidative stress. 1,25(OH)2D3 promotes stem cell proliferation and drives the differentiation of neural stem cells into oligodendrocytes, which carry out remyelination. 
  • 307
  • 24 Oct 2023
Topic Review
Neuroprotective Effects of Epigallocatechin-3-Gallate in Alzheimer’s Disease
Alzheimer’s disease (AD) is the most common cause of dementia, characterised by a marked decline of both memory and cognition, along with pathophysiological hallmarks including amyloid beta peptide (Aβ) accumulation, tau protein hyperphosphorylation, neuronal loss and inflammation in the brain. Additionally, oxidative stress caused by an imbalance between free radicals and antioxidants is considered one of the main risk factors for AD, since it can result in protein, lipid and nucleic acid damage and exacerbate Aβ and tau pathology. Green tea, and its main bioactive compound, epigallocatechin-3-gallate (EGCG), have been targeted as a plausible option for the modulation of AD. Specifically, EGCG acts as an antioxidant by regulating inflammatory processes involved in neurodegeneration such as ferroptosis and microglia-induced cytotoxicity and by inducing signalling pathways related to neuronal survival. Furthermore, it reduces tau hyperphosphorylation and aggregation and promotes the non-amyloidogenic route of APP processing, thus preventing the formation of Aβ and its subsequent accumulation.
  • 438
  • 20 Oct 2023
Topic Review
Insulin Resistance Causes Alzheimer’s Disease
Alzheimer’s disease (AD) is a neurodegenerative disorder associated with cognitive decline. Despite worldwide efforts to find a cure, no proper treatment has been developed yet, and the only effective countermeasure is to prevent the disease progression by early diagnosis. The reason why new drug candidates fail to show therapeutic effects in clinical studies may be due to misunderstanding the cause of AD. Regarding the cause of AD, the most widely known is the amyloid cascade hypothesis, in which the deposition of amyloid beta and hyperphosphorylated tau is the cause. However, many new hypotheses were suggested. Among them, based on preclinical and clinical evidence supporting a connection between AD and diabetes, insulin resistance has been pointed out as an important factor in the development of AD. 
  • 255
  • 16 Oct 2023
Topic Review
Executive Functions and Theory of Mind in Aging
Social cognition is essential for maintaining relationships throughout life, with Theory of Mind (ToM) as its central component. ToM encompasses both cognitive and affective processes, enabling individuals to decipher concealed social cues and make moral judgments within various social contexts. ToM is a current topic of interest investigated in diverse age-related conditions, such as Mild Cognitive Impairment (MCI), a transitional stage between healthy and pathological aging. Recognizing ToM difficulties is crucial, as they can significantly impact decision-making and social interactions while also serving as valuable indicators for tracking disease progression. However, assessing ToM poses challenges, given the variety of available tests and the ongoing debate about its connection with other cognitive abilities. Existing literature suggests that executive functions (EF) can influence ToM performance, but only a few studies have delved into this aspect deeply. Improving the understanding of the dynamics of ToM, its interaction with age-related changes, and its possible variations in MCI is critical to promoting social well-being and cognitive health in older people.
  • 324
  • 25 Oct 2023
Topic Review
Therapeutic Strategies for Pantothenate Kinase
The term neurodegeneration with brain iron accumulation (NBIA) brings together a broad set of progressive and disabling neurological genetic disorders in which iron is deposited preferentially in certain areas of the brain. Among NBIA disorders, the most frequent subtype is pantothenate kinase-associated neurodegeneration (PKAN) caused by pathologic variants in the PANK2 gene codifying the enzyme pantothenate kinase 2 (PANK2). 
  • 335
  • 10 Oct 2023
Topic Review
Expression and Regulation of INPP5D in  Alzheimer’s Disease
Alzheimer’s disease (AD) is the most common form of dementia, accounting for approximately 38.5 million cases of all-cause dementia. Microglial cells, the innate immune cells of the central nervous system (CNS), have long been established as guardians of the brain by providing neuroprotection and maintaining cellular homeostasis. A protein with a myriad of effects on various important signaling pathways that is expressed in microglia is the Src Homology 2 (SH2) domain-containing Inositol 5′ Phosphatase 1 (SHIP1) protein. Encoded by the INPP5D (Inositol Polyphosphate-5-Phosphatase D) gene, SHIP1 has diminutive effects on most microglia signaling processes. Polymorphisms of the INPP5D gene have been found to be associated with a significantly increased risk of AD.
  • 321
  • 09 Oct 2023
Topic Review
The Molecular Basis of Fragile X-Premutation-Associated Conditions
The premutation of the fragile X messenger ribonucleoprotein 1 (FMR1) gene is characterized by an expansion of the CGG trinucleotide repeats (55 to 200 CGGs) in the 5’ untranslated region and increased levels of FMR1 mRNA. Molecular mechanisms leading to fragile X-premutation-associated conditions (FXPAC) include cotranscriptional R-loop formations, FMR1 mRNA toxicity through both RNA gelation into nuclear foci and sequestration of various CGG-repeat-binding proteins, and the repeat-associated non-AUG (RAN)-initiated translation of potentially toxic proteins.
  • 415
  • 28 Sep 2023
Topic Review
TDP-43 Role in Chromatin Remodeling and Transcription
TDP-43 gained momentum in the neurodegeneration field when it was first discovered that almost all amyotrophic lateral sclerosis (ALS) cases and as many as half of frontotemporal dementia (FTD) cases present pathological ubiquitinated inclusions of TDP-43. Its involvement in chromatin silencing and nuclear/cytoplasmic shuttling constitute convergent key findings from several biological screens, and several crucial epigenetic factors appear to be able to modify TDP-43-induced degeneration. TDP-43 activity at the chromatin level and its implication in the regulation of DNA transcription and stability -such as DNA repair and regulation of retrotransposons activity- are further supported by a continuously growing amount of studies.
  • 542
  • 19 Sep 2023
Topic Review
One-Carbon Metabolism in Healthy Brain Aging
One-carbon (1C) metabolism is a key metabolic network that integrates nutritional signals with several processes in the human body. Dietary supplementation of 1C components, such as folic acid, vitamin B12, and choline are reported to have beneficial effects on normal and diseased brain function.
  • 357
  • 18 Sep 2023
Topic Review
Skull Stripping Methods
Skull stripping removes non-brain tissues from magnetic resonance (MR) images, but it is hard because of brain variability, noise, artifacts, and pathologies. The existing methods are slower and limited to a single orientation, mostly axial. Researchers' proposed and experimented method uses the modern and robust architecture of deep learning neural networks, viz., Mask–region convolutional neural network (RCNN) to learn, detect, segment, and to apply the mask on brain features and patterns from many thousands of brain MR images.
  • 231
  • 18 Sep 2023
  • Page
  • of
  • 49
>>