Bibliografie tematiche / Mitochondrial pathology

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Letteratura scientifica selezionata sul tema "Mitochondrial pathology"

Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 31 gennaio 2023

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Articoli di riviste sul tema "Mitochondrial pathology"

Sarnat, Harvey B., e José Marín-García. "Pathology of Mitochondrial Encephalomyopathies". Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 32, n. 2 (maggio 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 deficiency of Complex IV or of coenzyme-Q10. The selective loss of cytochrome-c-oxidase activity in scattered myofibers, particularly if accompanied by strong succinate dehydrogenase staining in these same fibres, is good evidence of mitochondrial cytopathy and often of a significant mtDNA mutation, though not specific for Complex IV disorders. Glycogen may be excessive in ragged-red zones. Ultrastructure provides morphological evidence of mitochondrial cytopathy, in axons and endothelial cells as well as myocytes. Abnormal axonal mitochondria may contribute to neurogenic atrophy of muscle, a secondary chronic feature. Quantitative determinations of respiratory chain enzyme complexes, with citrate synthase as an internal control, confirm the histochemical impressions or may be the only evidence of mitochondrial disease. Biological and technical artifacts may yield falsely low enzymatic activities. Genetic studies screen common point mutations in mtDNA. The brain exhibits characteristic histopathological alterations in mitochondrial diseases. Skin biopsy is useful for mitochondrial ultrastructure in smooth erector pili muscles and axons; skin fibroblasts may be grown in culture. Mitochondrial alterations occur in many nonmitochondrial diseases and also may be induced by drugs and toxins.

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Feng, Baoyi, Chenxi Jin, Zhenzhe Cheng, Xingle Zhao, Zhuoer Sun, Xiaofei Zheng, Xiang Li, Tingting Dong, Yong Tao e Hao Wu. "Mitochondrial Dysfunction and Therapeutic Targets in Auditory Neuropathy". Neural Plasticity 2020 (28 agosto 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 pharmacological therapy were studied in neurodegeneration, providing new insights in mitochondrion-targeted treatment of AN. In this review, we summarized mitochondrial biological functions related to SGNs and discussed interaction between mitochondrial dysfunction and AN, as well as existing mitochondrion treatment for SNHL. Pharmaceutical exploration to protect mitochondrion dysfunction is a feasible and effective therapeutics for AN.

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Picone, Pasquale, Domenico Nuzzo, Luca Caruana, Valeria Scafidi e 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 oxidative stress are one of the primary events in the insurgence of the pathology. Here, we examine structural and functional mitochondrial changes in presence of Aβ. In particular we review data concerning Aβimport into mitochondrion and its involvement in mitochondrial oxidative stress, bioenergetics, biogenesis, trafficking, mitochondrial permeability transition pore (mPTP) formation, and mitochondrial protein interaction. Moreover, the development of AD therapy targeting mitochondria is also discussed.

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Nevzorova, V. A., V. M. Chertok, T. A. Brodskaya, P. A. Selyukova e N. V. Zakharchuk. "Mitochondrial dysfunction and vascular aging in comorbid pathology". Pacific Medical Journal, n. 1 (25 marzo 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 mitochondrial protein. In addition to morphological changes, the function of mitochondria is oppressed, at the same time the activity of their proteins and enzymes decreases. Changes in the functions of mitochondria can be secondary in response to various stimuli and are associated with a violation of their structure and a change in activity in response to specific genetic and phenotypic conditions. Reprogramming of mitochondrial biogenesis occupies a central position in the theory of cellular aging and is one of the targets for interventions in prolonging active longevity.

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Abramov, Andrey Y., e Plamena R. Angelova. "Cellular mechanisms of complex I-associated pathology". Biochemical Society Transactions 47, n. 6 (26 novembre 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 cardio and muscular pathologies and diseases of the central nervous system. Despite such a clear involvement of complex I deficiency in numerous disorders, the molecular and cellular mechanisms leading to the development of pathology are not very clear. In this review, we summarise how lack of activity of complex I could differentially change mitochondrial and cellular functions and how these changes could lead to a pathology, following discrete routes.

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Schumacker, Paul T., Mark N. Gillespie, Kiichi Nakahira, Augustine M. K. Choi, Elliott D. Crouser, Claude A. Piantadosi e Jahar Bhattacharya. "Mitochondria in lung biology and pathology: more than just a powerhouse". American Journal of Physiology-Lung Cellular and Molecular Physiology 306, n. 11 (1 giugno 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 mitochondrial DNA relative to its involvement as a damage-associated molecular pattern driving adverse lung and systemic cell responses in severe illness or trauma. Finally, emerging strategies for replenishing normal populations of mitochondria after damage, either through promotion of mitochondrial biogenesis or via mitochondrial transfer, are discussed.

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Patterson, Kathleen. "Mitochondrial Muscle Pathology". Pediatric and Developmental Pathology 7, n. 6 (novembre 2004): 629–32. http://dx.doi.org/10.1007/s10024-004-5051-4.

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

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Jhun, Bong, Jin O-Uchi, Stephanie Adaniya, Michael Cypress e Yisang Yoon. "Adrenergic Regulation of Drp1-Driven Mitochondrial Fission in Cardiac Physio-Pathology". Antioxidants 7, n. 12 (18 dicembre 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 for mitochondrial and cellular functions including bioenergetics, reactive oxygen species (ROS) generation, spatiotemporal dynamics of Ca2+ signaling, cell growth, and death in the mammalian cell- and tissue-specific manners. Recent reports show that a mitochondrial fission protein, dynamin-like/related protein 1 (DLP1/Drp1), is post-translationally modified via cell signaling pathways, which control its subcellular localization, stability, and activity in cardiomyocytes/heart. In this review, we summarize the possible molecular mechanisms for causing post-translational modifications (PTMs) of DLP1/Drp1 in cardiomyocytes, and further discuss how these PTMs of DLP1/Drp1 mediate abnormal mitochondrial morphology and mitochondrial dysfunction under adrenergic signaling activation that contributes to the development and progression of HF.

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Luna-Sánchez, Marta, Patrizia Bianchi e Albert Quintana. "Mitochondria-Induced Immune Response as a Trigger for Neurodegeneration: A Pathogen from Within". International Journal of Molecular Sciences 22, n. 16 (7 agosto 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 mitochondrial content into the cytosol, which triggers an unwanted cellular immune response. Mitochondrial nucleic acids (mtDNA and mtRNA) can interact with the same cytoplasmic sensors that are specialized in recognizing genetic material from pathogens. High-energy demanding cells, such as neurons, are highly affected by deficits in mitochondrial function. Notably, mitochondrial dysfunction, neurodegeneration, and chronic inflammation are concurrent events in many severe debilitating disorders. Interestingly in this context of pathology, increasing number of studies have detected immune-activating mtDNA and mtRNA that induce an aberrant production of pro-inflammatory cytokines and interferon effectors. Thus, this review provides new insights on mitochondria-driven inflammation as a potential therapeutic target for neurodegenerative and primary mitochondrial diseases.

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Tesi sul tema "Mitochondrial pathology"

Blaikie, Frances H., e 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 cations are selectively accumulated by mitochondria within cells due to the mitochondria membrane potential. This thesis presents the synthesis and characterization of mitochondria targeted membrane uncoupler, cyclic nitroxide and alkyl thionitrite derivatives, all of which had the potential to influence reactive oxygen species. The biological analysis of these compounds is also presented. A triphenylphosphonium derivative of the membrane uncoupler 2,4-dinitrophenol (DNP) was anticipated to act as a self regulating protonophore. The DNP moiety would influence the scale of the membrane potential while the triphenylphosphonium cation would respond to the membrane potential. These two factors would combine so that as the membrane potential was dissipated by the uncoupler, the phosphonium cation would be released from the mitochondria and the effect of the uncoupler would thereby be nullified until the membrane potential had increased again. The compound was prepared by nitration of 3-(4-hydroxyphenyl)propyl triphenylphosphonium bromide. An untargeted derivative was also prepared by nitration of 3-(4-hydroxyphenyl)-1-propanol. Unfortunately, while this compound had appropriate acidity and lipophilicity to act as a membrane uncoupler, and did enter mitochondria in response to the membrane potential, it did not act as an uncoupler. A chemically stable targeted cyclic nitroxide based on Tempol was prepared following literature procedure, although other synthetic routes were also trialled. This compound was shown to concentrate in mitochondria in response to the membrane potential, was reduced by ubiquinol of the coenzyme Q pool, acted as a superoxide dismutase mimetic, and protected membranes against lipid peroxidation. A mitochondria targeted thionitrite or nitric oxide (NO) donor was anticipated to exhibit an effect on respiration at low oxygen concentrations as the released NO interacted with aspects of the respiratory chain. The alkyl thionitrites were synthesised from appropriate thiol precursors, several of which were prepared. Two targeted alkyl thionitrites were prepared with primary or tertiary carbon arrays next to the thionitrite functionality. Another targeted thionitrite, based on S-nitroso-N-acetylpenicillamine (SNAP), was also prepared. These compounds were difficult to characterise because of issues surrounding their stability. However, modified high resolution positive ion electrospray mass spectrometry in combination with HPLC and NMR was used to identify the compounds and to gauge the purity of the samples. Initial biological investigations verified that the primary alkylthionitrite derivative accumulated in mitochondria, released NO, and had an effect on respiration at low oxygen concentrations.

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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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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 osteogenesis following a spinal fusion is correlated with mitochondrial function of bone marrow stem cells. While the decline of bone with aging has been well studied, we were the first to find a concomitant decline in mitochondrial function in bone tissue. The most common mechanism of mitochondrial dysfunction is opening of the mitochondrial permeability transition pore (MPTP), a non-selective proteinaceous pore on the inner mitochondrial membrane, positively regulated by the protein cyclophilin D (CypD). Our CypD knockout mouse model has protected mitochondrial function in bone tissue and no decline in bone quality during aging. While we did show that protecting mitochondrial function is beneficial to age-associated bone loss, our ovariectomy model in the CypD knockout mouse did not show any protection. Thus, age-related and estrogen-related bone loss are likely controlled through different mechanisms. Overall, this work has shown the importance of mitochondrial metabolism in bone health and should be further explored as a new avenue for therapeutic interventions.

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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.
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.
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.
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.
Fibroblasts from a patient with facioscapulohumeral disease (FSHD), showed reduced oxidation of alanine and succinate through the ETC.
A fourth patient, with decreased activity in several complexes in muscle and liver, was found to have a heteroplasmic mtDNA population in fibroblasts.
These studies exemplify the heterogeneity of mitochondrial myopathies and demonstrate the utility of fibroblasts in the investigation of these disorders.

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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%) of all the papers which are included in this application are either first author or senior author publications. Mitochondrial respiratory chain disease exhibits marked clinical and genetic heterogeneity, often requiring the study of clinically-relevant, post-mitotic tissues to make a diagnosis which in many cases is made difficult on account of the peculiarities of mitochondrial genetics. Understanding this phenotypic diversity and elucidating the basic molecular mechanisms leading to cellular dysfunction continues to be challenging, with progress in the development of curative therapies hampered by our inability to manipulate the mitochondrial genome, and difficulties in obtaining alternative models of disease other than patients with pathogenic mtDNA mutations. . In an attempt to submit a cohesive application, the papers have been organised into relevant sections, beginning with general reviews of the clinical, biochemical and molecular features of mitochondrial genetic disease (Section A) followed by sections on the investigation and laboratory diagnosis of mitochondrial disease including epidemiology (Sections 8-0). The largest collection of papers document the molecular investigation of mitochondrial disorders, many describing novel mutations and disease mechanisms associated with both mtDNA- encoded and nuclear mitochondrial genes (Sections E-K). The next section describe studies investigating the role of somatic mtDNA abnormalities in neurodegenerative disease, cancer and ageing pathologies - including marking stem cell populations (Section L) - before a series of original research articles and invited reviews that focus on pharmacological and gene therapy strategies for the treatment of patients with mtDNA disease (Section M).

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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 PCR in three groups: 27 presumed HIV-negative, 89 HIV-infected, NRTI-treated and 62 HIV-infected treatment-naive children. Multivariate analysis was used to identify variables independently associated with mtDNA depletion. Results: Mean mt:nDNA ratios were lower (P < 0.001) at 77% of control in the HIVinfected antiretroviral treatment (ART) NaÃ¯ve group and 73% of control in the ART group, but not different between the two HIV-infected groups. Mt:nDNA ratios were negatively associated with age (P = 0.029), HIV status (P < 0.0001) and Log10 of the HIV-1 viral load (P = 0.035) and positively associated with CD4 % (p = 0.032). A 6 stavudine vs zidovudine based regimen was associated with lower but not significant levels of mtDNA (P = 0.1). Conclusions: Depletion of whole blood mtDNA in children is associated independently with HIV-infection and markers of HIV infection severity, and does not improve with either stavudine or zidovudine based ART despite virological control, suggesting that these agents also deplete mtDNA.

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Libri sul tema "Mitochondrial pathology"

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

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Gary, Fiskum, a cura di. Mitochondrial physiology and pathology. New York: Van Nostrand Reinhold, 1986.

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

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F, Palmieri, a cura di. 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., e Suleiman M. -Saadeh, a cura di. Mitochondria: The dynamic organelle. New York: Springer, 2007.

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Anna, Gvozdjáková, a cura di. 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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Capitoli di libri sul tema "Mitochondrial pathology"

Buchet, K., e 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., e 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 e 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., e 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, e 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 e 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 e 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 e 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., e 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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Atti di convegni sul tema "Mitochondrial pathology"

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 e 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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Abstract (sommario):

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 where animals present early amyloid pathology but no memory impairment - mimicking the human preclinical AD. Methods: We used high-resolution respirometry to assess mitochondrial oxidative phosphorylation capacity (OXPHOS), electron transfer capacity (ET), respiratory control ratio (RCR) and reserve capacity (R) in brain homogenates of male and female F344-AD and WT rats (n = 6-8, per group). Results: The results were analyzed by Welch’s t test: 1. Frontal cortex a)OXPHOS (p=0.307); b)ET (p=0.99); c)RCR (p=0.138); d)R (p=0.482). 2. Hippocampus a)OXPHOS (p=0.446); b)ET (p=0.409); c)RCR (p=0.952); d)R (p=0.503). Conclusion: In conclusion, at 6-7 months, changes in the respirometry in the brain of F344-AD rats were not observed. We hypothesize that these measures will be altered at older ages.

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