Relevant bibliographies by topics / Mitochondrial pathology

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Mitochondrial pathology'

Author: Grafiati
Published: 4 June 2021
Last updated: 31 January 2023

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Journal articles on the topic "Mitochondrial pathology"

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Sarnat, Harvey B., and José Marín-García. "Pathology of Mitochondrial Encephalomyopathies." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 32, no. 2 (May 2005): 152–66. http://dx.doi.org/10.1017/s0317167100003929.

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ABSTRACT:Muscle biopsy provides the best tissue to confirm a mitochondrial cytopathy. Histochemical features often correlate with specific syndromes and facilitate the selection of biochemical and genetic studies. Ragged-red fibres nearly always indicate a combination defect of respiratory complexes I and IV. Increased punctate lipid within myofibers is a regular feature of Kearns-Sayre and PEO, but not of MELAS and MERRF. Total deficiency of succinate dehydrogenase indicates a severe defect in Complex II; total absence of cytochrome-c-oxidase activity in all myofibres correlates with a severe
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Feng, Baoyi, Chenxi Jin, Zhenzhe Cheng, Xingle Zhao, Zhuoer Sun, Xiaofei Zheng, Xiang Li, Tingting Dong, Yong Tao, and Hao Wu. "Mitochondrial Dysfunction and Therapeutic Targets in Auditory Neuropathy." Neural Plasticity 2020 (August 28, 2020): 1–10. http://dx.doi.org/10.1155/2020/8843485.

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Sensorineural hearing loss (SNHL) becomes an inevitable worldwide public health issue, and deafness treatment is urgently imperative; yet their current curative therapy is limited. Auditory neuropathies (AN) were proved to play a substantial role in SNHL recently, and spiral ganglion neuron (SGN) dysfunction is a dominant pathogenesis of AN. Auditory pathway is a high energy consumption system, and SGNs required sufficient mitochondria. Mitochondria are known treatment target of SNHL, but mitochondrion mechanism and pathology in SGNs are not valued. Mitochondrial dysfunction and pharmacologica
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Picone, Pasquale, Domenico Nuzzo, Luca Caruana, Valeria Scafidi, and Marta Di Carlo. "Mitochondrial Dysfunction: Different Routes to Alzheimer’s Disease Therapy." Oxidative Medicine and Cellular Longevity 2014 (2014): 1–11. http://dx.doi.org/10.1155/2014/780179.

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Mitochondria are dynamic ATP-generating organelle which contribute to many cellular functions including bioenergetics processes, intracellular calcium regulation, alteration of reduction-oxidation potential of cells, free radical scavenging, and activation of caspase mediated cell death. Mitochondrial functions can be negatively affected by amyloidβpeptide (Aβ), an important component in Alzheimer’s disease (AD) pathogenesis, and Aβcan interact with mitochondria and cause mitochondrial dysfunction. One of the most accepted hypotheses for AD onset implicates that mitochondrial dysfunction and o
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Nevzorova, V. A., V. M. Chertok, T. A. Brodskaya, P. A. Selyukova, and N. V. Zakharchuk. "Mitochondrial dysfunction and vascular aging in comorbid pathology." Pacific Medical Journal, no. 1 (March 25, 2022): 10–16. http://dx.doi.org/10.34215/1609-1175-2022-1-10-16.

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Cardiovascular diseases take a leading position in the structure of mortality in modern society. Most diseases are characterized by uncontrolled processes of oxidative stress, proteolysis, tissue and cellular hypoxia, which cause endothelial dysfunction. Tissue and cellular hypoxia accumulated with mitochondrial reactive forms of oxygen damaging lipoproteins, proteins, nucleic acids plays an important role in the pathogenesis of vascular aging. Cellular aging is characterized by a decrease in the number of mitochondria, a decrease in the number of copies of mitochondrial DNA, and the loss of m
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Abramov, Andrey Y., and Plamena R. Angelova. "Cellular mechanisms of complex I-associated pathology." Biochemical Society Transactions 47, no. 6 (November 26, 2019): 1963–69. http://dx.doi.org/10.1042/bst20191042.

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Mitochondria control vitally important functions in cells, including energy production, cell signalling and regulation of cell death. Considering this, any alteration in mitochondrial metabolism would lead to cellular dysfunction and the development of a disease. A large proportion of disorders associated with mitochondria are induced by mutations or chemical inhibition of the mitochondrial complex I — the entry point to the electron transport chain. Subunits of the enzyme NADH: ubiquinone oxidoreductase, are encoded by both nuclear and mitochondrial DNA and mutations in these genes lead to ca
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Schumacker, Paul T., Mark N. Gillespie, Kiichi Nakahira, Augustine M. K. Choi, Elliott D. Crouser, Claude A. Piantadosi, and Jahar Bhattacharya. "Mitochondria in lung biology and pathology: more than just a powerhouse." American Journal of Physiology-Lung Cellular and Molecular Physiology 306, no. 11 (June 1, 2014): L962—L974. http://dx.doi.org/10.1152/ajplung.00073.2014.

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An explosion of new information about mitochondria reveals that their importance extends well beyond their time-honored function as the “powerhouse of the cell.” In this Perspectives article, we summarize new evidence showing that mitochondria are at the center of a reactive oxygen species (ROS)-dependent pathway governing the response to hypoxia and to mitochondrial quality control. The potential role of the mitochondrial genome as a sentinel molecule governing cytotoxic responses of lung cells to ROS stress also is highlighted. Additional attention is devoted to the fate of damaged mitochond
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Patterson, Kathleen. "Mitochondrial Muscle Pathology." Pediatric and Developmental Pathology 7, no. 6 (November 2004): 629–32. http://dx.doi.org/10.1007/s10024-004-5051-4.

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Sengers, R. C. A., and A. M. Stadhouders. "Secondary mitochondrial pathology." Journal of Inherited Metabolic Disease 10, S1 (March 1987): 98–104. http://dx.doi.org/10.1007/bf01812850.

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Jhun, Bong, Jin O-Uchi, Stephanie Adaniya, Michael Cypress, and Yisang Yoon. "Adrenergic Regulation of Drp1-Driven Mitochondrial Fission in Cardiac Physio-Pathology." Antioxidants 7, no. 12 (December 18, 2018): 195. http://dx.doi.org/10.3390/antiox7120195.

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Abnormal mitochondrial morphology, especially fragmented mitochondria, and mitochondrial dysfunction are hallmarks of a variety of human diseases including heart failure (HF). Although emerging evidence suggests a link between mitochondrial fragmentation and cardiac dysfunction, it is still not well described which cardiac signaling pathway regulates mitochondrial morphology and function under pathophysiological conditions such as HF. Mitochondria change their shape and location via the activity of mitochondrial fission and fusion proteins. This mechanism is suggested as an important modulator
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Luna-Sánchez, Marta, Patrizia Bianchi, and Albert Quintana. "Mitochondria-Induced Immune Response as a Trigger for Neurodegeneration: A Pathogen from Within." International Journal of Molecular Sciences 22, no. 16 (August 7, 2021): 8523. http://dx.doi.org/10.3390/ijms22168523.

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Symbiosis between the mitochondrion and the ancestor of the eukaryotic cell allowed cellular complexity and supported life. Mitochondria have specialized in many key functions ensuring cell homeostasis and survival. Thus, proper communication between mitochondria and cell nucleus is paramount for cellular health. However, due to their archaebacterial origin, mitochondria possess a high immunogenic potential. Indeed, mitochondria have been identified as an intracellular source of molecules that can elicit cellular responses to pathogens. Compromised mitochondrial integrity leads to release of m
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Dissertations / Theses on the topic "Mitochondrial pathology"

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Blaikie, Frances H., and n/a. "Synthesis and characterisation of probes that influence mitochondrial function." University of Otago. Department of Chemistry, 2008. http://adt.otago.ac.nz./public/adt-NZDU20080212.091116.

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The production of reactive oxygen species by mitochondria is implicated in mitochondrial dysfunction associated with a range of diseases and ageing. In addition, reactive oxygen species produced by mitochondria are involved in redox signalling pathways that modulate a number of cell processes. Mitochondria targeted antioxidants comprised of an antioxidant moiety linked to a lipophilic triphenylphosphonium cation have recently been used to decrease oxidative damage to mitochondria and to investigate the involvement of mitochondrial reactive oxygen species in redox signalling. These lipophilic c
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Renken, Christian Wolfgang. "The structure of mitochondria /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2004. http://wwwlib.umi.com/cr/ucsd/fullcit?p3141929.

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Jiang, Sirui. "Mitochondrial Dynamic Abnormalities in Alzheimer's Diease." Case Western Reserve University School of Graduate Studies / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=case1536608714970424.

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Shum, Laura C. "Mitochondrial Metabolism in Bone Physiology and Pathology." Thesis, University of Rochester, 2018. http://pqdtopen.proquest.com/#viewpdf?dispub=10792056.

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<p> Worldwide, 1 in 3 women and 1 in 5 men over age 50 will experience fractures due to a decline in bone quality. Elucidating the mechanisms for declining bone quality can lead to better therapeutics. A vital, yet overlooked aspect of bone health is the role of mitochondrial metabolism in both bone physiology and pathology. We have found that the ability of stem cells to differentiate into bone forming osteoblasts is sensitive to mitochondrial dysfunction, and therefore preserving mitochondrial function is essential to maintaining bone quality. In human patient samples, we found that osteogen
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Hanson, Bonnie Jean. "Protein based methods for the identification and classification of mitochondrial disorders /." view abstract or download file of text, 2001. http://wwwlib.umi.com/cr/uoregon/fullcit?p3018367.

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Thesis (Ph. D.)--University of Oregon, 2001.<br>Typescript. Includes vita and abstract. Includes bibliographical references (leaves 96-103). Also available for download via the World Wide Web; free to University of Oregon users.
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Oglesbee, Devin. "Improving the diagnosis of mitochondrial diseases : application of monoclonal antibody technologies to NADH:ubiquinone oxidoreductase and cytochrome c oxidase defects /." view abstract or download file of text, 2004. http://wwwlib.umi.com/cr/uoregon/fullcit?p3136436.

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Thesis (Ph. D.)--University of Oregon, 2004.<br>Typescript. Includes vita and abstract. Includes bibliographical references (leaves 113-119). Also available for download via the World Wide Web; free to University of Oregon users.
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Slipetz, Deborah M. "Characterization of mutations in pediatric mitochondrial myopathies." Thesis, McGill University, 1990. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=60101.

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Mitochondrial myopathies are a group of diverse neuromuscular disorders. Defects in electron transport chain (ETC) subunits have been implicated in pediatric and adult onset cases. Skin fibroblasts from four patients were studied to elucidate the biochemical defects.<br>Cells from two patients with ETC complex I deficiency, showed reduced oxidation of alanine with normal oxidation of succinate. Analysis of complex I subunits indicated deficient synthesis of the 20 kDa subunit in the severely affected patient. In the milder patient, subunit abnormalities were not detected.<br>Fibroblasts from a
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Malik, Safarina Golfiani 1963. "Human disorder of energy transduction : molecular pathology." Monash University, Dept. of Biochemistry and Molecular Biology, 2001. http://arrow.monash.edu.au/hdl/1959.1/8335.

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Taylor, Robert William. "Mitochondrial respiratory chain dysfunction in human pathology : investigation, pathogenicity and treatment." Thesis, University of Newcastle Upon Tyne, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.577189.

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The work presented in this thesis comprises 100 peer-reviewed publications, mostly original research papers but some key review articles are included, which highlight my ongoing research in understanding the role of mitochondrial respiratory chain dysfunction and mitochondrial DNA (mtDNA) mutation in human pathologies over a twenty year period, and in no small part have contributed to the development of my laboratory as a national referral centre in the UK for diagnostic biochemical and molecular genetic testing, funded by the NHS Specialist Commissioners. A significant proportion (at least 50
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van, der Watt George Frederick. "Whole Blood Mitochondrial DNA Depletion in Human Immunodeficiency Virus-Infected Children." Master's thesis, University of Cape Town, 2010. http://hdl.handle.net/11427/2705.

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Background: Nucleoside reverse transcriptase inhibitors (NRTIs) interfere with mitochondrial DNA polymerase gamma causing significant toxic effects, including fatal lactic acidosis. Little is known about mitochondrial DNA (mtDNA) in human immunodeficiency virus (HIV) infected children who face a lifetime exposure to these agents. We performed a cross sectional observation of mtDNA levels in whole blood in a pediatric population to ascertain the relationship between mtDNA, NRTI regimens and parameters of HIV-infection severity. Methods: Whole blood mt:nDNA ratios were determined by real-time PC
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Books on the topic "Mitochondrial pathology"

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Mitochondria. 2nd ed. Hoboken, N.J: John Wiley & Sons, 2008.

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Gary, Fiskum, ed. Mitochondrial physiology and pathology. New York: Van Nostrand Reinhold, 1986.

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N, Gellerich Frank, Zierz S, and Colloquium on Mitochondria and Myopathies (1st : 1995 : Halle an der Saale, Germany), eds. Detection of mitochondrial diseases. Dordrecht: Kluwer Academic, 1997.

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F, Palmieri, ed. Thirty years of progress in mitochondrial bioenergetics and molecular biology: Proceedings of the 23rd Bari meeting on bioenergetics, International Symposium on Thirty Years of Progress in Mitochondrial Bioenergetics and Molecular Biology : in honour of Professor E. Quagliariello's 70th birthday, Bari, Italy, 7-10 October 1994. Amsterdam: Elsevier, 1995.

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W, Schaffer S., and Suleiman M. -Saadeh, eds. Mitochondria: The dynamic organelle. New York: Springer, 2007.

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Anna, Gvozdjáková, ed. Mitochondrial medicine: Mitochondrial metabolism, diseases, diagnosis and therapy. Dordrecht: Springer, 2008.

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Mitochondrial signaling in health and disease. Boca Raton: Taylor & Francis/CRC Press, 2012.

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Balcells, Cristy. Living well with mitochondrial disease: A handbook for patients, parents, and families. Bethesda, MD: Woodbine House, 2012.

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Mitochondrial bioenergetics: Methods and protocols. New York: Humana Press, 2012.

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Mitochondrial dysfunction and oxidativedamage in neurodegenerative diseases. New York: Springer, 1995.

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Book chapters on the topic "Mitochondrial pathology"

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Buchet, K., and C. Godinot. "ATPase-ATP Synthase and Mitochondrial Pathology." In Mitochondrial Diseases, 129–42. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-59884-5_10.

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Poyau, A., and C. Godinot. "Cytochrome c Oxidase and Mitochondrial Pathology." In Mitochondrial Diseases, 115–27. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-59884-5_9.

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Duborjal, H., R. Beugnot, V. Procaccio, J. P. Issartel, and J. Lunardi. "Structure, Function and Pathology of Complex I." In Mitochondrial Diseases, 73–86. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-59884-5_6.

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Lestienne, P., and C. Desnuelle. "Complex II or Succinate: Quinone Oxidoreductase and Pathology." In Mitochondrial Diseases, 87–95. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-59884-5_7.

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Bai, Renkui, and Jaimie D. Higgs. "Mitochondrial Disorders." In Molecular Pathology in Clinical Practice, 139–59. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-19674-9_10.

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Litvak, S., M. Hernould, E. Zabaleta, V. Blanc, D. Begu, I. Kurek, A. Breiman, X. Jordana, A. Mouras, and A. Araya. "Plant Cytoplasmic Male Sterility: A Mitochondrial Pathology and Its Biotechnological Application." In Mitochondrial Diseases, 327–41. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-59884-5_25.

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Genova, Maria Luisa, Milena Merlo Pich, Andrea Bernacchia, Cristina Bianchi, Annalisa Biondi, Carla Bovina, Anna Ida Falasca, Gabriella Formiggini, Giovanna Parenti Castelli, and Giorgio Lenaz. "The Mitochondrial Production of Reactive Oxygen Species in Relation to Aging and Pathology." In Mitochondrial Pathogenesis, 86–100. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-662-41088-2_10.

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Jacobs, Howard T. "Mitochondrial ATP Synthase: Structure, Biogenesis and Pathology." In Organellar Proton-ATPases, 103–61. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-662-22265-2_5.

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Bárcena, Clea, Pablo Mayoral, Pedro M. Quirós, and Carlos López-Otín. "Physiological and Pathological Functions of Mitochondrial Proteases." In Proteases in Physiology and Pathology, 3–25. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-2513-6_1.

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Neginskaya, Maria A., and Evgeny V. Pavlov. "Inorganic Polyphosphate in Mitochondrial Energy Metabolism and Pathology." In Inorganic Polyphosphates, 15–26. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-01237-2_2.

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Conference papers on the topic "Mitochondrial pathology"

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Hill, Marcus, Mojtaba Fazli, Rachel Mattson, Meekail Zain, Andrew Durden, Allyson Loy, Barbara Reaves, et al. "Spectral Analysis of Mitochondrial Dynamics: A Graph-Theoretic Approach to Understanding Subcellular Pathology." In Python in Science Conference. SciPy, 2020. http://dx.doi.org/10.25080/majora-342d178e-00d.

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"Mitochondrial dysfunction and redox balance alterations in the development of AD-like pathology in OXYS rats." In Bioinformatics of Genome Regulation and Structure/ Systems Biology. institute of cytology and genetics siberian branch of the russian academy of science, Novosibirsk State University, 2020. http://dx.doi.org/10.18699/bgrs/sb-2020-334.

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Soares, Carolina, Débora G. Souza, Andreia Silva da Rocha, Luiza Machado, Bruna Bellaver, and Eduardo R. Zimmer. "BRAIN ENERGETICS EVALUATION IN EARLY STAGES OF AMYLOID PATHOLOGY IN A RAT MODEL OF ALZHEIMER’S DISEASE." In XIII Meeting of Researchers on Alzheimer's Disease and Related Disorders. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1980-5764.rpda086.

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Background: Transgenic models of Alzheimer’s disease (AD) overexpress human APP, PS1 or PS2 mutations. These models present amyloid-beta pathology but do not recapitulate the complexity of AD. Interestingly, the transgenic rat model TgF344-AD, which overpresses human APP and PS1 mutations, seems to follow a more similar disease progression, manifesting progressive tau tangle-like pathology and late cognitive impairment. Yet, whether they develop energy metabolism changes as we see in AD remains unclear. Objective: Here, we investigated brain bioenergetics in 6-7 months F344-AD/WT rats, an age
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