دانلود و نمایش مقالات مرتبط با Neurodegeneration::صفحه 1
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نتیجه جستجو - Neurodegeneration

تعداد مقالات یافته شده: 7
ردیف عنوان نوع
1 Assessing the neurotoxicity of the carbamate methomyl in Caenorhabditis elegans with a multi-level approach
ارزیابی سمیت عصبی کاربامات متومیل در Caenorhabditis elegans با رویکرد چند سطحی-2021
The neurotoxicity and developmental effects of a widely applied insecticide (methomyl) was investigated by amulti-level approach (behavior and biometry, biochemical alterations and neurodegeneration) in Caenorhabditis elegans upon a short-term exposure (1 h) and a post-exposure period (48 h). The 1-h exposure to sub-lethalconcentrations of methomyl (lower than 0.320 g L—1; i.e. below the estimated LC10) triggered significant changes on motor behavior and development impairment. The type of movement was significantly altered in methomyl-exposed worms, as well as biometric parameters (worms frequently idle and moving more backwards than controls; small body area, length and wavelength). These effects were followed by an increase of acetyl- choline levels. Interestingly, after the 48-h recovery period, movement of previously exposed worms was similar to controls, and a concentration-dependent reversion of biometric endpoints was recorded, pointing out the transient action of the carbamate in line with an apparent absence of cholinergic neurons damage. This study provided new insight on the neurotoxicity of methomyl by showing that effects on movement and development were transient, and apparently did not result in neurodegeneration in cholinergic neurons. Moreover, these findings reinforced the advantages of using C. elegans in a multi-level approach for pesticide effects assessment.
Keywords: Caenorhabditis elegans | Methomyl | Behavior | Acetylcholine | Neurodegeneration
مقاله انگلیسی
2 What electrophysiology tells us about Alzheimer’s disease: a window into the synchronization and connectivity of brain neurons
آنچه الکتروفیزیولوژی در مورد بیماری آلزایمر به ما می گوید: پنجره ای برای هماهنگ سازی و اتصال نورون های مغز-2020
Electrophysiology provides a real-time readout of neural functions and network capability in different brain states, on temporal (fractions of milliseconds) and spatial (micro, meso, and macro) scales unmet by other methodologies. However, current international guidelines do not endorse the use of electroencephalographic (EEG)/magnetoencephalographic (MEG) biomarkers in clinical trials performed in patients with Alzheimer’s disease (AD), despite a surge in recent validated evidence. This position paper of the ISTAART Electrophysiology Professional Interest Area endorses consolidated and translational electrophysiological techniques applied to both experimental animal models of AD and patients, to probe the effects of AD neuropathology (i.e., brain amyloidosis, tauopathy, and neurodegeneration) on neurophysiological mechanisms underpinning neural excitation/inhibition and neurotransmission as well as brain network dynamics, synchronization, and functional connectivity, reflecting thalamocortical and corticocortical residual capacity. Converging evidence shows relationships between abnormalities in EEG/MEG markers and cognitive deficits in groups of AD patients at different disease stages. The supporting evidence for the application of electrophysiology in AD clinical research as well as drug discovery pathways warrants an international initiative to include the use of EEG/MEG biomarkers in the main multicentric projects planned in AD patients, to produce conclusive findings challenging the present regulatory requirements and guidelines for AD studies.
Keywords: The Alzheimer’s Association International | Society to Advance Alzheimer’s Research | and Treatment (ISTAART) | Alzheimer’s disease (AD) | Electroencephalography and | magnetoencephalography (EEG and MEG) | Resting-state condition | Event-related potentials and magnetic fields | Preclinical and clinical research
مقاله انگلیسی
3 Apolipoproteins AI and E are associated with neuroaxonal injury to gray matter in multiple sclerosis
آپولیپوپروتئین های AI و E همراه با آسیب عصبی آکسون ماده خاکستری در بیماری ام اس-2020
Purpose To investigate the associations between longitudinal changes in lipid biomarkers and serum neurofilament (sNfL) levels in multiple sclerosis (MS) neurodegeneration and disease progression. Methods 5-year prospective, longitudinal study included 75 relapsing-remitting MS (RR-MS) and 37 progressive- MS (P-MS) patients. sNfL, plasma total cholesterol (TC), high-density (HDL-C) and low-density (LDL-C) lipoprotein cholesterol, apolipoproteins (Apo), ApoA-I, Apo-II, ApoB, ApoC-II and ApoE were measured at baseline and 5-years. Annual percent changes in whole brain volume (PBVC), gray matter volume (PGMVC) and cortical volume (PCVC) were obtained from MRI at baseline and 5-years. Results sNfL levels at 5-year follow-up were associated with ApoE at follow-up (p = 0.014), age at follow-up, body mass index (p<0.001) and RR vs. P-MS status at follow-up. APOE4 allele was associated with greater sNfL levels at 5-years (p = 0.022) and pronounced in the P-MS group. PGMVC and PCVC were associated with percent changes in HDL-C (p = 0018 and p < 0.001, respectively) and ApoA-I (p = 0.0073 and p = 0.006). PGMVC and PCVC remained associated with percent change in HDL-C (p = 0.0024 and p < 0.001, respectively) after sNfL was included as a predictor. Conclusions HDL-C percent change is associated with decreased gray matter atrophy after adjusting for baseline sNfL.
Keywords: Cholesterol | High density lipoprotein | Hdl | Apolipoproteins | Neurofilaments
مقاله انگلیسی
4 Proteotoxicity and mitochondrial dynamics in aging diabetic brain
Proteotoxicity و پویایی میتوکندری در پیری مغز دیابتی-2020
Impaired neuronal proteostasis is a salient feature of both aging and protein misfolding disorders. Amyloidosis, a consequence of this phenomena is observed in the brains of diabetic patients over the chronic time period. These toxic aggregates not only cause age-related decline in proteostasis, but also dwindle its ability to increase or restore the chaperones in response to any stressful condition. Mitochondria acts as the main source of energy regulation and many metabolic disorders such as diabetes have been associated with altered oxidative phosphorylation (OxPhos) and redox imbalance in the mitochondria. The mitochondrial unfolded protein response (UPRmt) acts as a mediator for maintaining the mitochondrial protein homeostasis and quality control during such conditions. Over a long time period, these responses start shutting off leading to proteotoxic stress in the neurons. This reduces the buffering capacity of protein network signalling during aging, thereby increasing the risk of neurodegeneration in the brain. In this review, we focus on the proteotoxic stress that occurs as an amalgamation of diabetes and aging, as well as the impact of mitochondrial dysfunction on the neuronal survival affecting the diabetic brain and its long term consequences on the memory changes.
Keywords: Proteotoxicity | Aging | Diabetes | Mitochondrial biogenesis | Mitophagy | Mitochondrial unfolded protein response | (UPRmt )
مقاله انگلیسی
5 DNAJB6, a Key Factor in Neuronal Sensitivity to Amyloidogenesis
DNAJB6 ، یک عامل اصلی در حساسیت عصبی به آمیلوئیدوژنز است-2020
CAG-repeat expansions in at least eight different genes cause neurodegeneration. The length of the extended polyglutamine stretches in the corresponding proteins is proportionally related to their aggregation propensity. Although these proteins are ubiquitously expressed, they predominantly cause toxicity to neurons. To understand this neuronal hypersensitivity, we generated induced pluripotent stem cell (iPSC) lines of spinocerebellar ataxia type 3 and Huntington’s disease patients. iPSC generation and neuronal differentiation are unaffected by polyglutamine proteins and show no spontaneous aggregate formation. However, upon glutamate treatment, aggregates form in neurons but not in patient-derived neural progenitors. During differentiation, the chaperone network is drastically rewired, including loss of expression of the antiamyloidogenic chaperone DNAJB6. Upregulation of DNAJB6 in neurons antagonizes glutamate-induced aggregation, while knockdown of DNAJB6 in progenitors results in spontaneous polyglutamine aggregation. Loss of DNAJB6 expression upon differentiation is confirmed in vivo, explaining why stem cells are intrinsically protected against amyloidogenesis and protein aggregates are dominantly present in neurons.
مقاله انگلیسی
6 Brain banking in low and middle-income countries: Raison Dêtre for the Ibadan Brain Ageing, Dementia And Neurodegeneration (IBADAN) Brain Bank Project
بانکداری مغز در کشورهایی با درآمد کم و متوسط: Raison Dêtre برای پیری مغز Ibadan ، زوال عقل و (Ibadan ) مغز پروژه بانک نورونها-2019
Brain banks are biorepositories of central nervous system (CNS) tissue including fixed and frozen whole brains, brain biopsies and spinal cord, as well as body fluids comprising the cerebrospinal fluid (CSF) and blood stored for research purposes. Though several independent brain banks exist in high income countries, only five low- and middle - income countries (LMIC) have brain banks. The African continent is yet to establish a formalized brain bank despite its huge human genomic diversity, ageing of her populations with concomitant increases in ageing – associated brain disorders and differential phenotypic expression and outcomes of brain disorders. Cellular and molecular clinicopathological studies are vital to shaping our understanding of the interaction between racial (genetic) and geographical (environmental) factors in the natural history and mechanisms of disease, and unravelling frameworks of diagnostic biomarkers, and new therapeutic and preventative interventions. The Ibadan Brain Ageing, Dementia And Neurodegeneration (IBADAN) Brain Bank, the first organized brain tissue biorepository in sub - Saharan Africa, is set up to accrue, process and store unique brain tissues for future research into a broad spectrum of neurological and psychiatric disorders. The potential unique discoveries and research breakthroughs will benefit people of African ancestry and other ancestral populations.
Keywords: Brain Banking | Nigeria | Africa | LMIC
مقاله انگلیسی
7 Reprogramming neurodegeneration in the big data era
برنامه ریزی مجدد نورونها دوران داده های بزرگ-2018
Recent genome-wide association studies (GWAS) have identified numerous genetic risk variants for late-onset Alzheimer’s disease (AD) and Parkinson’s disease (PD). However, deciphering the functional consequences of GWAS data is challenging due to a lack of reliable model systems to study the genetic variants that are often of low penetrance and non-coding identities. Pluripotent stem cell (PSC) technologies offer unprecedented opportunities for molecular phenotyping of GWAS variants in human neurons and microglia. Moreover, rapid technological advances in whole-genome RNA sequencing and epigenome mapping fuel comprehensive and unbiased investigations of molecular alterations in PSC derived disease models. Here, we review and discuss how integrated studies that utilize PSC technologies and genome wide approaches may bring new mechanistic insight into the pathogenesis of AD and PD.
مقاله انگلیسی
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