Search results for "NEURODEGENERATION"
showing 10 items of 268 documents
β-Amyloid-induced activation of Caspase-3 in primary cultures of rat neurons
2000
It is known that beta-amyloid peptide (Abeta) contributes to the neurodegeneration in Alzheimer's disease (AD) and operates through activation of an apoptotic pathway. Apoptotic signal is driven by a family of cysteine proteases called caspases. The beta-amyloid precursor protein (APP) is directly and efficiently cleaved by caspases during apoptosis, resulting in elevated beta-amyloid peptide formation. Cerebellar neurons from rat pups were treated with the aged Abeta(25-35) at 1 and 5 microM and fluorescence assays of caspase activity performed over 4 days. We observed an increase in caspase activity after 48 h treatment in both 1 and 5 microM treated cells, then (72-96 h) caspase activity…
The emerging role of miRNA-132/212 cluster in neurologic and cardiovascular diseases: Neuroprotective role in cells with prolonged longevity
2021
Abstract miRNA-132/212 are small regulators of gene expression with a function that fulfills a vital function in diverse biological processes including neuroprotection of cells with prolonged longevity in neurons and the cardiovascular system. In neurons, miRNA-132 appears to be essential for controlling differentiation, development, and neural functioning. Indeed, it also universally promotes axon evolution, nervous migration, plasticity as well, it is suggested to be neuroprotective against neurodegenerative diseases. Moreover, miRNA-132/212 disorder leads to neural developmental perturbation, and the development of degenerative disorders covering Alzheimer’s, Parkinson’s, and epilepsy’s …
Impaired calcium homeostasis in aged hippocampal neurons
2009
Abstract Development of neurodegenerative diseases such as Alzheimer's and Parkinson's disease is strongly age-associated. The impairment of calcium homeostasis is considered to be a key pathological event leading to neuronal dysfunction and cell death. However, the exact impact of aging on calcium homeostasis in neurons remains largely unknown. In the present work we have investigated intracellular calcium levels in cultured primary hippocampal neurons from young (2 months) and aged (24 months) rat brains. Upon stimulation with glutamate or hydrogen peroxide aged neurons in comparison to young neurons demonstrated an increased vulnerability to these disease-related toxins. Measurement of c…
Emerging contributions of formyl peptide receptors to neurodegenerative diseases.
2021
Abstract Inflammation is a central element of many neurodegenerative diseases. Formyl peptide receptors (FPRs) can trigger several receptor-dependent signal transduction pathways that play a key role in neuroinflammation and neurodegeneration. They are chemotactic receptors that help to regulate pro- and anti-inflammatory responses in most mammals. FPRs are primarily expressed in the immune and nervous systems where they interact with a complex pattern of pathogen-derived and host-endogenous molecules. Mounting evidence points towards a contribution of FPRs – via neuropathological ligands such as Amyloid beta, and neuroprotective ligands such as Humanin, Lipoxin A4, and Annexin A1 – to mult…
Oxidative stress in Alzheimer’s Disease: Implications for Prevention and Therapy
2006
Oxidative stress is a marker of neurodegeneration and has been recently shown to be also involved in the early stages of the pathogenesis of various neurodegenerative disorders. In general, all biomolecules of the cell can be oxidized and thereby damaged. Consequently, the concept of neuroprotection by antioxidants has been developed. In many cases the direct scavanging of free radicals have been used as a strategy to prevent oxidative stress damage and a variety of physiological and synthetic antioxidant molecules have been identified and synthesized including the female sex homone estrogen. In Alzheimer’s Disease amyloid-β protein on its way to brain deposition can also induce oxidative c…
Neuronal cell cycle: the neuron itself and its circumstances.
2015
Neurons are usually regarded as postmitotic cells that undergo apoptosis in response to cell cycle reactivation. Nevertheless, recent evidence indicates the existence of a defined developmental program that induces DNA replication in specific populations of neurons, which remain in a tetraploid state for the rest of their adult life. Similarly, de novo neuronal tetraploidization has also been described in the adult brain as an early hallmark of neurodegeneration. The aim of this review is to integrate these recent developments in the context of cell cycle regulation and apoptotic cell death in neurons. We conclude that a variety of mechanisms exists in neuronal cells for G1/S and G2/M check…
Preparation and characterization of extracts argania spinosa and argan oil and evaluation of their neuroprotective effects in vivo and in vitro
2016
من بين الزيوت الطبيعية أثار زيت أركان الكثير من الاهتمام. فقد استخدم زيت الأركان في الطب التقليدي، من قبل نساء البربرللعناية بالجسم و الشعر، و لمنع بعض الأمراض القلب و الأوعية الدموية . يتميز زيت الأركان بوظائفه التي تخص خفض الكوليسترول، مكافحة داء السكري ومكافحة التكاثر في خطوط الخلايا السرطانية البشرية للبروستات. يعتبر زيت اركان غنيا بالأحماض الدهنية غير المشبعة، البوليفينول، التوكوفيرول و الستيرول .هذه المواد تجعله مادة مضادة للأكسدة.يتركز دور مضادات الأكسدة الغذائية في وظيفة الجهاز العصبي وبعض الأمراض المرتبطة بالعمر على فيتامين E الذي يعتبر المكون الرئيسي لزيت أركان . الهدف من هذا العمل هو أولا دراسة كيميائية لنبتة اركان وتقييم القوة المضادة للأكسدة لمقتطفات هذه النبتة مع توصيف شامل لت…
Senataxin defective in ataxia oculomotor apraxia type 2 is involved in the defence against oxidative DNA damage
2007
Adefective response to DNA damage is observed in several human autosomal recessive ataxias with oculomotor apraxia, including ataxia-telangiectasia. We report that senataxin, defective in ataxia oculomotor apraxia (AOA) type 2, is a nuclear protein involved in the DNA damage response. AOA2 cells are sensitive to H2O2, camptothecin, and mitomycin C, but not to ionizing radiation, and sensitivity was rescued with full-length SETX cDNA. AOA2 cells exhibited constitutive oxidative DNA damage and enhanced chromosomal instability in response to H2O2. Rejoining of H2O2-induced DNA double-strand breaks (DSBs) was significantly reduced in AOA2 cells compared to controls, and there was no evidence fo…
Sensory neuropathy with bone destruction due to a mutation in the membrane-shaping atlastin GTPase 3.
2014
Many neurodegenerative disorders present with sensory loss. In the group of hereditary sensory and autonomic neuropathies loss of nociception is one of the disease hallmarks. To determine underlying factors of sensory neurodegeneration we performed whole-exome sequencing in affected individuals with the disorder. In a family with sensory neuropathy with loss of pain perception and destruction of the pedal skeleton we report a missense mutation in a highly conserved amino acid residue of atlastin GTPase 3 (ATL3), an endoplasmic reticulum-shaping GTPase. The same mutation (p.Tyr192Cys) was identified in a second family with similar clinical outcome by screening a large cohort of 115 patients …
Role of Hsp70 in Multiple Sclerosis: An Overview
2019
For many years heat shock protein 70 (Hsp70) was considered exclusively an intracellular chaperone contributing to protein proteostasis and in apoptotic pathway block. Lately it has been demonstrated that Hsp70 is actively released in the extracellular environment, thereby promoting the activation of the immune system by stimulating innate and adaptive responses through the activation of APCs. Its expression in the nervous system is induced in a variety of pathological conditions. Emerging evidences displayed that Hsp70 is a critical regulator in normal neural cells. Multiple sclerosis (MS) is an autoimmune disease of the central nervous system (CNS) directed against myelin antigens. In thi…