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Topic Review
Gender Differences in Cannabis Use
Gender differences in psychiatric disorders and drug use are well known. Cannabis is the most widely used illegal drug among young people. In recent years, its use has been related to the development of psychiatric pathologies; however, few studies have incorporated the gender perspective as of yet. Men have a higher prevalence using cannabis; however, women show a faster transition from recreational use to compulsive use, higher levels of craving with more relapses, and higher prevalence of dual pathology. Clinical studies clearly show the existence of gender differences in psychiatric symptoms associated with cannabis use. Although these results are not conclusive, they seem to indicate a higher vulnerability of women in the development of psychosis and anxiety, while men seem to be more vulnerable to developing depressive symptoms with long-term cannabis misuses. 
  • 1.6K
  • 02 Apr 2022
Topic Review
SF1 Neurons
SF1 neurons in the ventromedial hypothalamus are a specific lead in the brain’s ability to sense glucose levels and conduct insulin and leptin signaling in energy expenditure and glucose homeostasis.
  • 1.6K
  • 22 Jun 2021
Topic Review
CNS Glial Cells FA Synthesis
The central nervous system (CNS) has an exceptionally high lipid content. The brain contains the highest diversity of lipids than any other organ. Fatty acids (FA) are essential monomeric components that define the structural diversity of lipids and determine their functional properties in the CNS. FAs and their metabolites are critical for brain homeostasis and influence many neural functions, including cell survival, neurogenesis and synaptogenesis. Glial cells are a highly heterogeneous population of cells and predominate the mammalian brain. Astrocytes, oligodendrocytes and microglia are the major types of glial cells in the CNS. Their main function is to sustain a homeostatic environment for neuronal circuits, providing not only structural or trophic support but also controlling neuronal function and plasticity. To do so, glial cells heavily rely on transient and temporal changes in the FA and lipid metabolism.
  • 1.6K
  • 23 Aug 2021
Topic Review
Neurodegeneration
The human body is highly complex and comprises a variety of living cells and extracellular material, which forms tissues, organs, and organ systems. Human cells tend to turn over readily to maintain homeostasis in tissues. However, postmitotic nerve cells exceptionally have an ability to regenerate and be sustained for the entire life of an individual, to safeguard the physiological functioning of the central nervous system. For efficient functioning of the CNS, neuronal death is essential, but extreme loss of neurons diminishes the functioning of the nervous system and leads to the onset of neurodegenerative diseases. Neurodegenerative diseases range from acute to chronic severe life-altering conditions like Parkinson’s disease and Alzheimer’s disease. Millions of individuals worldwide are suffering from neurodegenerative disorders with little or negligible treatment available, thereby leading to a decline in their quality of life. Neuropathological studies have identified a series of factors that explain the etiology of neuronal degradation and its progression in neurodegenerative disease. The onset of neurological diseases depends on a combination of factors that causes a disruption of neurons, such as environmental, biological, physiological, and genetic factors. 
  • 1.5K
  • 16 Jul 2021
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.
  • 1.5K
  • 06 Jun 2022
Topic Review
Microbiota–Gut–Brain Axis in Mood Disorders
The microbiota–gut–brain axis is a bidirectional communication pathway that enables the gut microbiota to communicate with the brain through direct and indirect signaling pathways to influence brain physiology, function, and even behavior. Several taxonomic changes in the gut microbiota have been reported in neurodevelopmental disorders, mood disorders such as anxiety and depression, and neurodegenerative disorders such as Alzheimer’s disease. 
  • 1.5K
  • 17 Feb 2022
Topic Review
KCNQ Channels
The broad distribution of voltage-gated potassium channels (VGKCs) in the human body makes them a critical component for the study of physiological and pathological function. Within the KCNQ family of VGKCs, these aqueous conduits serve an array of critical roles in homeostasis, especially in neural tissue.
  • 1.5K
  • 19 May 2022
Topic Review
Synaptotagmin Isoforms and SYT1 Function
Synaptic dysregulations often result in damaging effects on the central nervous system, resulting in a wide range of brain and neurodevelopment disorders that are caused by mutations disrupting synaptic proteins. Synaptotagmin-1 (SYT1), an identified synaptotagmin protein, plays an essential role in mediating the release of calcium-triggered neurotransmitters (NT) involved in regular synaptic vesicle exocytosis. 
  • 1.5K
  • 19 Oct 2022
Topic Review
Alpha-Synuclein in Neurons
Accumulation of the neuronal presynaptic protein alpha-synuclein within proteinaceous inclusions represents the key histophathological hallmark of a spectrum of neurodegenerative disorders, referred to by the umbrella term a-synucleinopathies. Even though alpha-synuclein is expressed predominantly in neurons, pathological aggregates of the protein are also found in the glial cells of the brain. In Parkinson’s disease and dementia with Lewy bodies, alpha-synuclein accumulates mainly in neurons forming the Lewy bodies and Lewy neurites, whereas in multiple system atrophy, the protein aggregates mostly in the glial cytoplasmic inclusions within oligodendrocytes. In addition, astrogliosis and microgliosis are found in the synucleinopathy brains, whereas both astrocytes and microglia internalize alpha-synuclein and contribute to the spread of pathology. The mechanisms underlying the pathological accumulation of alpha-synuclein in glial cells that under physiological conditions express low to non-detectable levels of the protein are an area of intense research. Undoubtedly, the presence of aggregated alpha-synuclein can disrupt glial function in general and can contribute to neurodegeneration through numerous pathways. 
  • 1.5K
  • 17 Jun 2021
Topic Review
Metal-Induced Mitochondrial Dysfunction
Metals are actively involved in multiple catalytic physiological activities. However, metal overload may result in neurotoxicity as it increases formation of reactive oxygen species (ROS) and elevates oxidative stress in the nervous system. Mitochondria are a key target of metal-induced toxicity, given their role in energy production. As the brain consumes a large amount of energy, mitochondrial dysfunction and the subsequent decrease in levels of ATP may significantly disrupt brain function, resulting in neuronal cell death and ensuing neurological disorders. 
  • 1.5K
  • 30 Jun 2021
Topic Review
Neuroprotective Role of Lactoferrin during Early Brain Development
Early adverse fetal environments can significantly disturb central nervous system (CNS) development and subsequently alter brain maturation. Nutritional status is a major variable to be considered during development and increasing evidence links neonate and preterm infant impaired brain growth with neurological and psychiatric diseases in adulthood. Breastfeeding is one of the main components required for healthy newborn development due to the many “constitutive” elements breastmilk contains. Maternal intake of specific nutrients during lactation may alter milk composition, thus affecting newborn nutrition and, potentially, brain development. Lactoferrin (Lf) is a major protein present in colostrum and the main protein in human milk, which plays an important role in the benefits of breastfeeding during postnatal development. It has been demonstrated that Lf has antimicrobial, as well as anti-inflammatory properties, and is potentially able to reduce the incidence of sepsis and necrotizing enterocolitis (NEC), which are particularly frequent in premature births. The anti-inflammatory effects of Lf can reduce birth-related pathologies by decreasing the release of pro-inflammatory factors and inhibiting premature cervix maturation (also related to commensal microbiome abnormalities) that could contribute to disrupting brain development. Pre-clinical evidence shows that Lf protects the developing brain from neuronal injury, enhances brain connectivity and neurotrophins production, and decreases inflammation in models of perinatal inflammatory challenge, intrauterine growth restriction (IUGR) and neonatal hypoxia-ischemia (HI). Lactoferrin has also been considered a potential biomarker of neurodegeneration and its mechanisms of action make it a good candidate to be tested in the prevention of neurodegenerative diseases.
  • 1.5K
  • 08 Aug 2022
Topic Review
α-Synuclein
The α-syn, encoded by the SNCA1/PARK1 gene, is a ubiquitous protein that is abundantly expressed in kidneys and blood cells, but highly enriched in the brain, particularly in the presynaptic terminals of the neocortex, hippocampus, substantia nigra (SN), thalamus, and cerebellum. Interestingly, it has been found expressed in the cytoplasm of astrocytes and oligodendrocytes in healthy individuals.
  • 1.5K
  • 12 Nov 2021
Topic Review
Fenamates for Neurodegenerative Disorders
Neurodegenerative disorders are desperately lacking treatment options. It is imperative that drug repurposing be considered in the fight against neurodegenerative diseases. Fenamates have been studied for efficacy in treating several neurodegenerative diseases. 
  • 1.5K
  • 06 May 2021
Topic Review
The Effects of Diets on the “Gut–Brain” Pathways
With depression becoming increasingly prevalent, being closely associated with stress, and many patients exhibiting resistance to current treatments, depression pathophysiology requires further elucidation. Recent research has shown complex bidirectional links between the brain and the gut, and the gut microbiota and the influence of diet is beginning to provide new clues to the complex nature of this disorder. It is well known that diet is a key modulator of gut microbial composition. In humans, good quality plant-based diets such as the Mediterranean diet have been shown to reduce pathogenic bacteria in the gut, increase Bifidobacterium and Clostridium, as well as lower the risk of depression, while poorer quality diets such as the Western diet have been shown to reduce Lactobacillus in the gut, reduce overall gut microbial diversity and have been associated with increased depression risk. Evaluating the effects of diets on the brain-to-gut and gut-to-brain mechanisms in animal models of stress and depression may aid in the elucidation of the pathophysiology of depression and may provide novel therapeutic approaches. 
  • 1.5K
  • 21 Feb 2022
Topic Review
DNA-Repair Pathways: Links to Neurodegeneration
Genomic integrity is maintained by DNA repair and the DNA damage response (DDR). Defects in certain DNA repair genes give rise to many rare progressive neurodegenerative diseases (NDDs), such as ocular motor ataxia, Huntington disease (HD), and spinocerebellar ataxias (SCA). A possible causative role for DNA damage and DNA repair in the pathogenesis of common, late-onset NDDs is less well established, although DDR defects are emerging as possible culprits in diseases like AD, PD, and ALS. Whether targeting DNA repair or the DDR may be developed into therapeutic options against NDDs remains to be clarified.
  • 1.5K
  • 18 Jun 2021
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. 
  • 1.5K
  • 10 Jun 2022
Topic Review
The Gut-Immune-Brain Axis in Inflammatory Bowel Disease
Inflammatory bowel disease (IBD) is a chronic inflammatory disease comprising two major clinical entities—Crohn’s disease (CD) and ulcerative colitis (UC). IBD incidence remains constantly high in industrialized countries and continuously rises in emerging economies. Importantly, IBD is associated with neuropsychiatric symptoms that strongly worsen IBD disease burden. Mounting evidence indicates that chronic gut inflammation induces a systemic immune response that might cause the CNS manifestation in IBD. In line with this, biologicals targeting inflammatory circuits exerted robust positive effects on depressive symptoms in many autoimmune diseases, and in IBD in particular. Therefore, research in recent years increasingly focused on the characterization of local and systemic immune reactions in IBD, and on entry routes of inflammatory cells and molecules into the CNS. The ultimate aim is to understand how the changes in the neuroimmune landscape impair the function of neurons to cause neuropsychiatric symptoms. In addition, the role of intestinal microbiota in the gut–immune–brain axis in IBD will be discussed. 
  • 1.5K
  • 18 Oct 2022
Topic Review
Brain Calcifications
Brain calcifications (BC) are intracranial calcium deposits localized in the brain parenchyma and its microvasculature. Their prevalence ranges from 1% in young individuals up to 38% in elderly subjects. Calcified areas are easily identified by clinicians as hyperdense alterations on brain CT. A certain degree of intracranial calcifications, particularly of the basal ganglia, pineal gland, choroid plexus, and habenula, can be considered a normal phenomenon associated with aging. Indeed, BC are often incidental findings on neuroimaging of asymptomatic individuals; however, they can also be associated with many genetic and acquired disorders. BC can be primary, as observed in several early- and late-onset genetic syndromes, or can be secondary to systemic alterations of phosphate–calcium metabolism (genetic and also acquired forms), intrauterine (e.g., TORCH) and post-natal infections (e.g., neurocysticercosis), hypoxic-ischemic injuries, toxic exposures (e.g., lead), brain tumors (e.g., oligodendrogliomas), and autoimmune disorders (e.g., systemic lupus erythematosus).
  • 1.5K
  • 10 Aug 2023
Topic Review
Modelling Parkinson’s Disease
Parkinson’s Disease (PD) is a chronic neurodegenerative disorder characterized by motor and non-motor symptoms, among which are bradykinesia, rigidity, tremor as well as mental symptoms such as dementia. 
  • 1.5K
  • 07 Jul 2021
Topic Review
Physiological Function of Alpha-Synuclein
Synucleinopathy underlies a wide spectrum of clinical syndromes, including Parkinson's disease (PD), Parkinson's disease dementia (PDD), dementia with Lewy bodies (DLB), multiple system atrophy (MSA), and pure autonomic failure (PAF). A common feature of these syndromes is alpha-synuclein (aS) aggregation and cellular inclusions.  In synucleinopathies, the formation of the distinct αS species is determined by the nature of the self-assembly processes, which is influenced by many factors including the SNCA mutation or multiplication, epigenetic regulation, post-translational modification, micro-environments, etc.  Both the oligomeric and fibrillar forms of αS are toxic to cells.  The detrimental effects of αS continue to grow as αS fibrils start to form LBs, which can cause mitochondrial disassembly, mitophagy, mitochondrial depolarization, and synaptic dysfunction that result in progressive neurodegeneration.  
  • 1.5K
  • 16 Sep 2023
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