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Stress model for neurodegenerative disorders

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https://www.readbyqxmd.com/read/28427412/lack-of-interleukin-13-receptor-%C3%AE-1-delays-the-loss-of-dopaminergic-neurons-during-chronic-stress
#1
Simone Mori, Shuei Sugama, William Nguyen, Tatiana Michel, M Germana Sanna, Manuel Sanchez-Alavez, Rigo Cintron-Colon, Gianluca Moroncini, Yoshihiko Kakinuma, Pamela Maher, Bruno Conti
BACKGROUND: The majority of Parkinson's disease (PD) cases are sporadic and idiopathic suggesting that this neurodegenerative disorder is the result of both environmental and genetic factors. Stress and neuroinflammation are among the factors being investigated for their possible contributions to PD. Experiments in rodents showed that severe chronic stress can reduce the number of dopaminergic neurons in the substantia nigra pars compacta (SNc); the same cells that are lost in PD. These actions are at least in part mediated by increased oxidative stress...
April 21, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/28423529/pif-promotes-brain-re-myelination-locally-while-regulating-systemic-inflammation-clinically-relevant-multiple-sclerosis-m-smegmatis-model
#2
Giuseppe Migliara, Martin Mueller, Alessia Piermattei, Chaya Brodie, Michael J Paidas, Eytan R Barnea, Francesco Ria
Neurologic disease diagnosis and treatment is challenging. Multiple Sclerosis (MS) is a demyelinating autoimmune disease with few clinical forms and uncertain etiology. Current studies suggest that it is likely caused by infection(s) triggering a systemic immune response resulting in antigen/non-antigen-related autoimmune response in central nervous system (CNS). New therapeutic approaches are needed. Secreted by viable embryos, PreImplantation Factor (PIF) possesses a local and systemic immunity regulatory role...
March 28, 2017: Oncotarget
https://www.readbyqxmd.com/read/28413833/beneficial-effects-of-a-pyrroloquinolinequinone-containing-dietary-formulation-on-motor-deficiency-cognitive-decline-and-mitochondrial-dysfunction-in-a-mouse-model-of-alzheimer-s-disease
#3
Darrell Sawmiller, Song Li, Takashi Mori, Ahsan Habib, David Rongo, Vedad Delic, Patrick C Bradshaw, R Douglas Shytle, Cyndy Sanberg, Paula Bickford, Jun Tan
Alzheimer's disease (AD), a progressive neurodegenerative disorder, is linked to oxidative stress, altered amyloid precursor protein (APP) proteolysis, tau hyperphosphorylation and the accumulation of amyloid-β (Aβ) plaques and neurofibrillary tangles (NFT). A growing body of evidence suggests that mitochondrial dysfunction can be a key promoter of all of these pathologies and predicts that restoration of mitochondrial function might be a potential therapeutic strategy for AD. Therefore, in the present study, we tested the beneficial effect of a nutraceutical formulation Nutrastem II (Nutra II), containing NT020 (a mitochondrial restorative and antioxidant proprietary formulation) and pyrroloquinolinequinone (PQQ, a stimulator of mitochondria biogenesis) in 5XFAD transgenic mice...
April 2017: Heliyon
https://www.readbyqxmd.com/read/28410533/protein-aggregation-into-insoluble-deposits-protects-from-oxidative-stress
#4
Anita Carija, Susanna Navarro, Natalia Sanchez de Groot, Salvador Ventura
Protein misfolding and aggregation have been associated with the onset of neurodegenerative disorders. Recent studies demonstrate that the aggregation process can result in a high diversity of protein conformational states, however the identity of the specific species responsible for the cellular damage is still unclear. Here, we use yeast as a model to systematically analyse the intracellular effect of expressing 21 variants of the amyloid-ß-peptide, engineered to cover a continuous range of intrinsic aggregation propensities...
April 4, 2017: Redox Biology
https://www.readbyqxmd.com/read/28405779/multidirectional-inhibition-of-cortico-hippocampal-neurodegeneration-by-kolaviron-treatment-in-rats
#5
Olayemi Joseph Olajide, Nnaemeka Tobechukwu Asogwa, Blessing Oluwapelumi Moses, Christiana Bidemi Oyegbola
Earliest signs of neurodegenerative cascades in the course of Alzheimer's disease (AD) are seen within the prefrontal cortex (PFC) and hippocampus, with pathological evidences in both cortical structures correlating with manifestation of behavioural and cognitive deficits. Despite the enormous problems associated with AD's clinical manifestations in sufferers, therapeutic advances for the disorder are still very limited. Therefore, this study examined cortico-hippocampal microstructures in models of AD, and evaluated the possible beneficial roles of kolaviron (Kv)-a biflavonoid complex in rats...
April 13, 2017: Metabolic Brain Disease
https://www.readbyqxmd.com/read/28389404/protective-role-of-apigenin-on-rotenone-induced-rat-model-of-parkinson-s-disease-suppression-of-neuroinflammation-and-oxidative-stress-mediated-apoptosis
#6
Chandran Anusha, Thangarajan Sumathi, Leena Dennis Joseph
Parkinson's disease (PD) is a neurodegenerative disorder characterized by the loss of dopaminergic neurons in the substantia nigra which is associated with oxidative stress, neuroinflammation and apoptosis. Apigenin (AGN), a non-mutagenic flavone found in fruits and vegetables, exhibits a variety of biological effects including anti-apoptotic, anti-inflammatory, and free radical scavenging activities. The current study was aimed to investigate the neuroprotective effects and molecular mechanisms of AGN in a rat model of PD induced by rotenone (ROT)...
April 4, 2017: Chemico-biological Interactions
https://www.readbyqxmd.com/read/28382744/exercise-and-bdnf-reduce-a%C3%AE-production-by-enhancing-%C3%AE-secretase-processing-of-app
#7
Saket M Nigam, Shaohua Xu, Joanna S Kritikou, Krisztina Marosi, Lennart Brodin, Mark P Mattson
Alzheimer's disease (AD) is an age-related neurodegenerative disorder characterized by aggregation of toxic forms of amyloid β peptide (Aβ). Treatment strategies have largely been focused on inhibiting the enzymes (β- and γ-secretases) that liberate Aβ from the amyloid precursor protein (APP). While evidence suggests that individuals who exercise regularly are at reduced risk for AD and studies of animal models demonstrate that running can ameliorate brain Aβ pathology and associated cognitive deficits, the underlying mechanisms are unknown...
April 6, 2017: Journal of Neurochemistry
https://www.readbyqxmd.com/read/28379216/nicorandil-attenuates-neuronal-mitochondrial-dysfunction-and-oxidative-stress-associated-with-murine-model-of-vascular-calcification
#8
Sriram Ravindran, Krithika Swaminathan, Abhinaya Ramesh, Gino A Kurian
Evidences suggest that the presence of chronic kidney disease (CKD) is associated with cerebrovascular diseases related cognitive decline in dialysis patients. As mitochondrial dysfunction is implicated in neurodegenerative disorders, we hypothesized that changes in brain mitochondria occur due to vascular calcification induced by renal failure and the opening of the mitochondrial potassium channel using nicorandil may prevent its dysfunction. Brain tissues from rats with vascular calcification were studied...
2017: Acta Neurobiologiae Experimentalis
https://www.readbyqxmd.com/read/28375739/mito-apocynin-prevents-mitochondrial-dysfunction-microglial-activation-oxidative-damage-and-progressive-neurodegeneration-in-mitopark-transgenic-mice
#9
Monica Langley, Anamitra Ghosh, Adhithiya Charli, Souvarish Sarkar, Muhammet Ay, Jie Luo, Jacek Zielonka, Timothy Brenza, Brian Bennett, Huajun Jin, Shivani Ghaisas, Benjamin Schlichtmann, Dongsuk Kim, Vellareddy Anantharam, Arthi Kanthasamy, Balaji Narasimhan, Balaraman Kalyanaraman, Anumantha G Kanthasamy
AIMS: Parkinson's disease (PD) is a neurodegenerative disorder characterized by progressive motor deficits and degeneration of dopaminergic neurons. Caused by a number of genetic and environmental factors, mitochondrial dysfunction and oxidative stress play a role in neurodegeneration in PD. By selectively knocking out mitochondrial transcription factor A (TFAM) in dopaminergic neurons, the transgenic MitoPark mice recapitulate many signature features of the disease, including progressive motor deficits, neuronal loss, and protein inclusions...
April 4, 2017: Antioxidants & Redox Signaling
https://www.readbyqxmd.com/read/28371411/generation-of-integration-free-induced-pluripotent-stem-cells-from-urine-derived-cells-isolated-from-individuals-with-down-syndrome
#10
Young M Lee, Bruna L Zampieri, Jonah J Scott-McKean, Mark W Johnson, Alberto C S Costa
Down syndrome (DS) is a genetic disorder caused by trisomy 21 (T21). Over the past two decades, the use of mouse models has led to significant advances in the understanding of mechanisms underlying various phenotypic features and comorbidities secondary to T21 and even informed the design of clinical trials aimed at enhancing the cognitive abilities of persons with DS. In spite of its success, this approach has been plagued by all the typical limitations of rodent modeling of human disorders and diseases. Recently, several laboratories have succeeded in producing T21 human induced pluripotent stem cells (T21-iPSCs) from individuals with DS, which is emerging as a promising complementary tool for the study of DS...
March 28, 2017: Stem Cells Translational Medicine
https://www.readbyqxmd.com/read/28363448/trauma-associated-sleep-disorder-a-parasomnia-induced-by-trauma
#11
REVIEW
Vincent Mysliwiec, Matthew S Brock, Jennifer L Creamer, Brian M O'Reilly, Anne Germain, Bernard J Roth
Nightmares and disruptive nocturnal behaviors that develop after traumatic experiences have long been recognized as having different clinical characteristics that overlap with other established parasomnia diagnoses. The inciting experience is typically in the setting of extreme traumatic stress coupled with periods of sleep disruption and/or deprivation. The limited number of laboratory documented cases and symptomatic overlap with rapid eye movement sleep behavior disorder (RBD) and posttraumatic stress disorder (PTSD) have contributed to difficulties in identifying what is a unique parasomnia...
January 30, 2017: Sleep Medicine Reviews
https://www.readbyqxmd.com/read/28361919/discovery-of-the-first-dual-gsk3%C3%AE-inhibitor-nrf2-inducer-a-new-multitarget-therapeutic-strategy-for-alzheimer-s-disease
#12
Isabel Gameiro, Patrycja Michalska, Giammarco Tenti, Ángel Cores, Izaskun Buendia, Ana I Rojo, Nikolaos D Georgakopoulos, Jesús M Hernández-Guijo, María Teresa Ramos, Geoffrey Wells, Manuela G López, Antonio Cuadrado, J Carlos Menéndez, Rafael León
The formation of neurofibrillary tangles (NFTs), oxidative stress and neuroinflammation have emerged as key targets for the treatment of Alzheimer's disease (AD), the most prevalent neurodegenerative disorder. These pathological hallmarks are closely related to the over-activity of the enzyme GSK3β and the downregulation of the defense pathway Nrf2-EpRE observed in AD patients. Herein, we report the synthesis and pharmacological evaluation of a new family of multitarget 2,4-dihydropyrano[2,3-c]pyrazoles as dual GSK3β inhibitors and Nrf2 inducers...
March 31, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28359739/2-4-dnp-improves-motor-function-preserves-medium-spiny-neuronal-identity-and-reduces-oxidative-stress-in-a-mouse-model-of-huntington-s-disease
#13
Bin Wu, Mali Jiang, Qi Peng, Gang Li, Zhipeng Hou, Ginger L Milne, Susumu Mori, Robert Alonso, John G Geisler, Wenzhen Duan
Huntington's disease (HD) is a neurodegenerative disorder caused by a CAG repeat expansion in the first exon of the gene huntingtin. There is no treatment to prevent or delay the disease course of HD currently. Oxidative stress and mitochondrial dysfunction have emerged as key determinants of the disease progression in HD. Therefore, counteracting mutant huntingtin (mHtt)-induced oxidative stress and mitochondrial dysfunction appears as a new approach to treat this devastating disease. Interestingly, mild mitochondrial uncoupling improves neuronal resistance to stress and facilitates neuronal survival...
March 28, 2017: Experimental Neurology
https://www.readbyqxmd.com/read/28337696/cerebral-dopamine-neurotrophic-factor-a-potential-therapeutic-agent-for-parkinson-s-disease
#14
REVIEW
Tingting Tang, Yong Li, Qian Jiao, Xixun Du, Hong Jiang
The application of neurotrophic factors (NTFs) is a promising therapeutic strategy for neurodegenerative disorders such as Parkinson's disease (PD). Many NTFs have been reported to enhance the survival, regeneration, and differentiation of neurons and to induce synaptic plasticity. However, because of their potential side-effects and low efficacy after clinical administration, more potent treatments for neurodegenerative disorders are being sought. Cerebral dopamine neurotrophic factor (CDNF), a newly-identified NTF homologous to mesencephalic astrocyte-derived NTF, is structurally and functionally different from other NTFs, providing new hope especially for PD patients...
March 23, 2017: Neuroscience Bulletin
https://www.readbyqxmd.com/read/28325755/loss-of-pink1-leads-to-metabolic-deficits-in-adult-neural-stem-cells-and-impedes-differentiation-of-newborn-neurons-in-the-mouse-hippocampus
#15
Sandeep Kumar Agnihotri, Ruifang Shen, Jihong Li, Xu Gao, Hansruedi Büeler
Emerging evidence suggests that mitochondrial dynamics regulates adult hippocampal neurogenesis (AHN). Although abnormal AHN has been linked to depression, anxiety, and cognitive dysfunction, which are features of neurodegenerative conditions, including Parkinson's disease (PD), the impact of mitochondrial deficits on AHN have not been explored previously in a model of neurodegeneration. Here, we used PTEN-induced kinase 1-deficient (PINK1(-/-) ) mice that lacked a mitochondrial kinase mutated in recessive familial PD...
March 21, 2017: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/28320183/ischemic-optic-neuropathy-as-a-model-of-neurodegenerative-disorder-a-review-of-pathogenic-mechanism-of-axonal-degeneration-and-the-role-of-neuroprotection
#16
REVIEW
Saba Khalilpour, Shahrzad Latifi, Ghazaleh Behnammanesh, Amin Malik Shah Abdul Majid, Aman Shah Abdul Majid, Ali Tamayol
Optic neuropathy is a neurodegenerative disease which involves optic nerve injury. It is caused by acute or intermittent insults leading to visual dysfunction. There are number of factors, responsible for optic neuropathy, and the optic nerve axon is affected in all type which causes the loss of retinal ganglion cells. In this review we will highlight various mechanisms involved in the cell loss cascades during axonal degeneration as well as ischemic optic neuropathy. These mechanisms include oxidative stress, excitotoxicity, angiogenesis, neuroinflammation and apoptosis following retinal ischemia...
April 15, 2017: Journal of the Neurological Sciences
https://www.readbyqxmd.com/read/28315978/the-hallucinogen-2-5-dimethoxy-4-iodoamphetamine-hydrochloride-activates-neurotrophin-receptors-in-a-neuronal-cell-line-and-promotes-neurites-extension
#17
Zoya Marinova, Susanne Walitza, Edna Grünblatt
Decreased neurotrophic factors expression and neurotrophin receptors signalling have repeatedly been reported in association with stress, depression, and neurodegenerative disorders. We have previously identified the hallucinogen 2,5-dimethoxy-4-iodoamphetamine hydrochloride (DOI) as protective against trophic deprivation-induced cytotoxicity in human neuroblastoma SK-N-SH cells and established the dependence of this effect on the 5-HT2A receptor, tyrosine kinases activity, and the extracellular signal-regulated kinase pathway...
March 18, 2017: Journal of Neural Transmission
https://www.readbyqxmd.com/read/28303372/ellagic-acid-ameliorates-learning-and-memory-deficits-in-a-rat-model-of-alzheimer-s-disease-an-exploration-of-underlying-mechanisms
#18
Zahra Kiasalari, Rana Heydarifard, Mohsen Khalili, Siamak Afshin-Majd, Tourandokht Baluchnejadmojarad, Elham Zahedi, Ashkan Sanaierad, Mehrdad Roghani
RATIONALE: Alzheimer's disease (AD) is a neurodegenerative disorder with irreversible loss of intellectual abilities. Current therapies for AD are still insufficient. OBJECTIVE: In this study, the effect of ellagic acid on learning and memory deficits was evaluated in intrahippocampal amyloid beta (Aβ25-35)-microinjected rats and its modes of action were also explored. METHODS: AD rat model was induced by bilateral intrahippocampal microinjection of Aβ25-35 and ellagic acid was daily administered (10, 50, and 100 mg/kg), and learning, recognition memory, and spatial memory were evaluated in addition to histochemical assessment, oxidative stress, cholinesterases activity, and level of nuclear factor-kappaB (NF-κB), Toll-like receptor 4 (TLR4), and nuclear factor (erythroid-derived 2)-like 2 (Nrf2)...
March 16, 2017: Psychopharmacology
https://www.readbyqxmd.com/read/28303260/evidence-for-an-additive-neurorestorative-effect-of-simultaneously-administered-cdnf-and-gdnf-in-hemiparkinsonian-rats-implications-for-different-mechanism-of-action
#19
Merja H Voutilainen, Francesca De Lorenzo, Polina Stepanova, Susanne Bäck, Li-Ying Yu, Päivi Lindholm, Eeva Pörsti, Mart Saarma, Pekka T Männistö, Raimo K Tuominen
Parkinson's disease (PD) is a neurodegenerative disorder associated with a progressive loss of dopaminergic (DAergic) neurons of the substantia nigra (SN) and the accumulation of intracellular inclusions containing α-synuclein. Current therapies do not stop the progression of the disease, and the efficacy of these treatments wanes over time. Neurotrophic factors (NTFs) are naturally occurring proteins promoting the survival and differentiation of neurons and the maintenance of neuronal contacts. CDNF (cerebral dopamine NTF) and GDNF (glial cell line-derived NTF) are able to protect DAergic neurons against toxin-induced degeneration in experimental models of PD...
January 2017: ENeuro
https://www.readbyqxmd.com/read/28294542/pras40-alleviates-neurotoxic-prion-peptide-induced-apoptosis-via-mtor-akt-signaling
#20
Wei Yang, Li-Feng Yang, Zhi-Qi Song, Syed Zahid Ali Shah, Yong-Yong Cui, Chao-Si Li, Hua-Fen Zhao, Hong-Li Gao, Xiang-Mei Zhou, De-Ming Zhao
AIMS: The proline-rich Akt substrate of 40-kDa (PRAS40) protein is a direct inhibitor of mTORC1 and an interactive linker between the Akt and mTOR pathways. The mammalian target of rapamycin (mTOR) is considered to be a central regulator of cell growth and metabolism. Several investigations have demonstrated that abnormal mTOR activity may contribute to the pathogenesis of several neurodegenerative disorders and lead to cognitive deficits. METHODS: Here, we used the PrP peptide 106-126 (PrP(106-126) ) in a cell model of prion diseases (also known as transmissible spongiform encephalopathies, TSEs) to investigate the mechanisms of mTOR-mediated cell death in prion diseases...
May 2017: CNS Neuroscience & Therapeutics
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