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Adolescence and Aging: Impact of Adolescence Inflammatory Stress and Microbiota Alterations on Brain Development, Aging, and Neurodegeneration.
Yahfoufi, N, Matar, C, Ismail, N
The journals of gerontology. Series A, Biological sciences and medical sciences. 2020;(7):1251-1257
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Abstract
Puberty/adolescence is a critical phase during neurodevelopment with numerous structural, neurochemical, and molecular changes occurring in response to genetic and environmental signals. A consequence of this major neuronal reorganizing and remodeling is a heightened level of vulnerability to stressors and immune challenges. The gut microbiota is a fundamental modulator of stress and immune responses and has been found to play a role in mental health conditions and neurodegenerative disorders. Environmental insults (stress, infection, neuroinflammation, and use of antibiotics) during adolescence can result in dysbiosis subsidizing the development of brain disorders later in life. Also, pubertal neuroinflammatory insults can alter neurodevelopment, impact brain functioning in an enduring manner, and contribute to neurological disorders related to brain aging, such as Alzheimer's disease, Parkinson's disease, and depression. Exposure to probiotics during puberty can mitigate inflammation, reverse dysbiosis, and decrease vulnerabilities to brain disorders later in life. The goal of this review is to reveal the consequences of pubertal exposure to stress and immune challenges on the gut microbiota, immune reactivity within the brain, and the risk or resilience to stress-induced mental illnesses and neurodegenerative disorders. We propose that the consumption of probiotics during adolescence contribute to the prevention of brain pathologies in adulthood.
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[Serum IgG antibodies to GD1a and GM1 gangliosides in elderly people].
Kolyovska, V
Biomeditsinskaia khimiia. 2016;(1):93-5
Abstract
Nowadays, the percentage of elderly people in society grows. Good nutrition and medical care help older people to have a normal life over 80 to 90 years. In the last ten years it is of critical importance to establish the clinical significance of serum IgG anti-GD1a and anti-GM1 ganglioside antibodies as potential biomarkers for neuronal damage in neurodegenerative diseases and immune-mediated neuropathies and demyelination. In the current study, the diagnostic values of IgG anti-GD1a and anti-GM1 antibodies were determined by the ELISA method in serum samples of 18 elderly patients (71-91 years). Significantly elevated serum IgG anti-GD1a and anti-GM1 antibodies titers were detected only in patients over 80 years. These data suggest that the immune-mediated neuropathies, neurodegeneration and demyelination in healthy elderly occur after 80 years old. Therefore, IgG anti-GD1a and anti-GM1 antibodies can serve as biomarkers, showing the nervous system dysfunction.
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[Molecular mechanism of idiopathic basal ganglia calcification].
Wang, C, Xu, X, Li, LL, Wang, T, Zhang, M, Shen, L, Tang, BS, Liu, JY
Yi chuan = Hereditas. 2015;(8):731-40
Abstract
Idiopathic basal ganglia calcification (IBGC), also known as Fahr’s disease, is an inheritable neurodegenerative syndrome characterized by mineral deposits in the basal ganglia and other brain regions. Patients with IBGC are often accompanied with movement disorders, cognitive impairment as well as psychiatric abnormalities. So far, no therapeutic drug has been developed for the treatment of IBGC. Recently, genetic studies have identified several genes associated with IBGC, including SLC20A2, PDGFRB, PDGFB, ISG15 and XPR1. Loss-of-function mutations in these genes have been associated with disturbance in phosphate homeostasis in brain regions, the dysfunction of blood-brain barrier as well as enhanced IFN-α/β immunity. In this review, we summarize the latest research progress in the studies on molecular genetics of IBGC, and discuss the molecular mechanisms underlying the pathophysiology of mutations of different genes.
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[Mechanisms of neurodegeneration in Alzheimer's disease].
Jovanović, Z
Medicinski pregled. 2012;(7-8):301-7
Abstract
INTRODUCTION Recent research into mechanisms of neurodegeneration in Alzheimer's disease has lead to a dramatic increase in our understanding of the mechanisms of cell death and neuroprotection. Alzheimer's disease is a complex disease with multiple etiological factors involved in disease pathogenesis. OXIDATIVE STRESS AND MITOCHONDRIAL DYSFUNCTION IN ALZHEIMER'S DISEASE Amyloid-beta peptide toxicity is mediated at least in part by oxidative stress. Anmyloid-beta peptide directly generates reactive oxygen species in the presence of redox-active metal ions. In Alzheimer's disease, oxidative stress is present early in pathogenesis and contributes to disease pathogenesis. Unlike other organs, the brain is especially vulnerable to reactive oxygen species due to neurons having relatively low levels of endogenous antioxidants. Overly abundant oxygen radicals cause the destruction of cellular macromolecules and participate in signaling mechanisms that result in apoptotic cell death. MICROGLIAL ACTIVATION AND NICOTINAMIDE ADENINE DINUCLEOTIDE PHOSPHATE OXIDASE IN ALZHEIMER'S DISEASE There is a wealth of evidence demonstrating that microglia, the resident innate immune cells in the brain, can become deleterious and damage neurons. Microglial activation causes neuron damage through the production of neurotoxic factors, such as reactive oxygen species and cytokines that are toxic to neurons. The neuron also has strong homeostatic mechanisms that can delay or prevent activation of apoptosis and necrosis. INSULIN RESISTANCE AND ALZHEIMER'S DISEASE Insulin plays a role in Alzheimer's disease, as it is involved in the metabolism of beta-amyloid. Hyperinsulinemia and type-2 diabetes mellitus results in an increased risk of developing Alzheimer's disease, but its implications when the disease is already well established remain unknown. Treatment of central insulin resistance may be a promising avenue, not only in metabolic syndrom, but also in Alzheimer's disease. CONCLUSION Increasing evidence suggests a role for oxidative stress, mitochondrial dysfunction, microglial activation and insulin resistance in pathogenesis of neurodegenerative diseases including Alzheimer's disease.
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Pathogens and chronic or long-term neurologic disorders.
Starakis, I, Panos, G, Koutras, A, Mazokopakis, EE
Cardiovascular & hematological disorders drug targets. 2011;(1):40-52
Abstract
Infections of the central nervous system may provoke glial and autoimmune responses but a definitive linkage between these infections and the pathogenesis of chronic neurologic disorders is still elusive. There are controversial reports implicating infectious agents in the pathogenetic mechanisms of chronic or long-term neurologic disorders, such as multiple sclerosis, amyotrophic lateral sclerosis, Parkinson's disease, Alzheimer's disease and autistic spectrum disorders, but the specific role of bacterial or viral infections in the pathogenesis of these medical entities has not been fully elucidated. Up till now, the evidence is distant from definite, but certain cases may be attributed to infections in the millieu of multiple toxic events such as trauma, nutritional deficits, immune dysregulation and excitotoxicity in genetically vulnerable indiniduals. There is an ongoing debate concering the direct involvement of various infectious agents in the neurodegenerative and neurobehavioral diseases pathogenesis and/or their contribution to the deterioration of the disease or co-morbidity in these patients. These patients are exceptionally difficult to be treated by using single therapeutic modalities, because their disese is multifocal and treatment is aimed to control signs and symptoms rather than the true causes of the disease and its progressive course. Furthermore, even if these causative links were indetifiable, our therapeutic interventions would come too late due to the irreversible damages at the time of the initiation of treatment. Our aim is to comprehensively review all available data suggesting that infections could be common antecedent events of progressive neurologic degenerative or behavioural diseases.