Relevant bibliographies by topics / Syndrome progeroïde

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

Academic literature on the topic 'Syndrome progeroïde'

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Published: 25 May 2024

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Journal articles on the topic "Syndrome progeroïde"

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De Barros, Paula Vitória Macêdo, Enrico Souza De Godoy, Lucas Rafael Ferreira Soares, and João Ricardo Mendes De Oliveira. "Searching for proper criteria to add new and rare conditions to the Progeroid Syndromes category." Brazilian Journal of Health Review 7, no. 1 (February 5, 2024): 4365–71. http://dx.doi.org/10.34119/bjhrv7n1-353.

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The progeroid syndromes represents a group of rare diseases that presents clinical aspects of physiological aging at early stages of life. These syndromes share many clinical features such as craniofacial features, skin, hair and nails alterations, neurodevelopment and motor disorders and premature-onset malignancies. Primrose syndrome is a rare autosomal dominant disorder caused by de novo heterozygous missense variants in ZBTB20 and exhibits as main clinical manifestations craniofacial features, intellectual disability, hypotonia, postnatal-onset macrocephaly, behavior abnormalities, progressive musculoskeletal and motor involvement and endocrine dysfunctions. Anchored in previous works that discussed the physiopathology and clinical spectrum of progeroid syndromes and also the molecular, genetic and clinical hallmarks of Primrose syndrome, this letter highlights the hypothesis that Primrose syndrome could be classified as a progeroid syndrome. This possibility might not only amplify our understanding of progeroid syndromes but also might have impact in the treatments available and offered to patients with rare diseases.
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Kungurtseva, A. L., and A. V. Vitebskaya. "Differential Diagnosis of Progeroid Neonatal Syndrome." Doctor.Ru 22, no. 7 (2023): 37–42. http://dx.doi.org/10.31550/1727-2378-2023-22-7-37-42.

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Aim. Аnalysis and synthesis of the literature data on the problem of differential diagnosis of neonatal progeroid syndrome. Key points. One of the rarest representatives of premature aging syndromes is neonatal progeroid syndrome (Wiedemann–Rautenstrauch syndrome). It is an ultra-orphan disease with autosomal recessive type of inheritance, associated with a mutation in the POLR3A, POLR3B, POLR3GL genes and characterized by congenital lipodystrophy and premature aging. The disease manifests from the first days of life: low body length and weight at birth, pronounced phenotypic features (pseudohydrocephaly, progeroid facial features, generalized lipodystrophy, neonatal incisors). Severe bronchopulmonary and skeletal damage is seen over the course of life, and average life expectancy ranges from 7 months to 2 years but can reach 27 years. The differential diagnosis is made with Hutchinson–Gilford syndrome (progeria), which clinical signs manifest at 1.5-2 years of age, and with Marfan-progeroid lipodystrophy, Fontaine syndrome, and Sekkel syndrome. Conclusion. Early diagnostics is necessary for predicting the course of the disease, selection of treatment, and determining of further management. Keywords: neonatal progeroid syndrome, Wiedemann–Rautenstrauch syndrome, premature aging syndromes
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Golounina, Olga O., Valentin V. Fadeev, and Zhanna E. Belaya. "Hereditary syndromes with signs of premature aging." Osteoporosis and Bone Diseases 22, no. 3 (June 1, 2020): 4–18. http://dx.doi.org/10.14341/osteo12331.

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Aging is a multi-factor biological process that inevitably affects everyone. Degenerative processes, starting at the cellular and molecular levels, gradually influence the change in the functional capabilities of all organs and systems. Progeroid syndromes (from Greek. progērōs prematurely old), or premature aging syndromes, represent clinically and genetically heterogeneous group of rare hereditary diseases characterized by accelerated aging of the body. Progeria and segmental progeroid syndromes include more than a dozen diseases, but the most clear signs of premature aging are evident in Hutchinson-Guilford Progeria Syndrome and Werner Syndrome. This review summarizes the latest scientific data reflecting the etiology and clinical picture of progeria and segmental progeroid syndromes in humans. Molecular mechanisms of aging are considered, using the example of progeroid syndromes. Modern possibilities and potential ways of influencing the mechanisms of the development of age-related changes are discussed. Further study of genetic causes, as well as the development of treatment for progeria and segmental progeroid syndromes, may be a promising direction for correcting age-related changes and increasing life expectancy.
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Rivera-Mulia, Juan Carlos, Romain Desprat, Claudia Trevilla-Garcia, Daniela Cornacchia, Hélène Schwerer, Takayo Sasaki, Jiao Sima, et al. "DNA replication timing alterations identify common markers between distinct progeroid diseases." Proceedings of the National Academy of Sciences 114, no. 51 (December 1, 2017): E10972—E10980. http://dx.doi.org/10.1073/pnas.1711613114.

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Progeroid syndromes are rare genetic disorders that phenotypically resemble natural aging. Different causal mutations have been identified, but no molecular alterations have been identified that are in common to these diseases. DNA replication timing (RT) is a robust cell type-specific epigenetic feature highly conserved in the same cell types from different individuals but altered in disease. Here, we characterized DNA RT program alterations in Hutchinson–Gilford progeria syndrome (HGPS) and Rothmund–Thomson syndrome (RTS) patients compared with natural aging and cellular senescence. Our results identified a progeroid-specific RT signature that is common to cells from three HGPS and three RTS patients and distinguishes them from healthy individuals across a wide range of ages. Among the RT abnormalities, we identified the tumor protein p63 gene (TP63) as a gene marker for progeroid syndromes. By using the redifferentiation of four patient-derived induced pluripotent stem cells as a model for the onset of progeroid syndromes, we tracked the progression of RT abnormalities during development, revealing altered RT of the TP63 gene as an early event in disease progression of both HGPS and RTS. Moreover, the RT abnormalities in progeroid patients were associated with altered isoform expression of TP63. Our findings demonstrate the value of RT studies to identify biomarkers not detected by other methods, reveal abnormal TP63 RT as an early event in progeroid disease progression, and suggest TP63 gene regulation as a potential therapeutic target.
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Osorio, Fernando G., Alejandro P. Ugalde, Guillermo Mariño, Xose S. Puente, José M. P. Freije, and Carlos López-Otín. "Cell autonomous and systemic factors in progeria development." Biochemical Society Transactions 39, no. 6 (November 21, 2011): 1710–14. http://dx.doi.org/10.1042/bst20110677.

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Progeroid laminopathies are accelerated aging syndromes caused by defects in nuclear envelope proteins. Accordingly, mutations in the LMNA gene and functionally related genes have been described to cause HGPS (Hutchinson–Gilford progeria syndrome), MAD (mandibuloacral dysplasia) or RD (restrictive dermopathy). Functional studies with animal and cellular models of these syndromes have facilitated the identification of the molecular alterations and regulatory pathways involved in progeria development. We have recently described a novel regulatory pathway involving miR-29 and p53 tumour suppressor which has provided valuable information on the molecular components orchestrating the response to nuclear damage stress. Furthermore, by using progeroid mice deficient in ZMPSTE24 (zinc metalloprotease STE24 homologue) involved in lamin A maturation, we have demonstrated that, besides these abnormal cellular responses to stress, dysregulation of the somatotropic axis is responsible for some of the alterations associated with progeria. Consistent with these observations, pharmacological restoration of the somatotroph axis in these mice delays the onset of their progeroid features, significantly extending their lifespan and supporting the importance of systemic alterations in progeria progression. Finally, we have very recently identified a novel progeroid syndrome with distinctive features from HGPS and MAD, which we have designated NGPS (Néstor–Guillermo progeria syndrome) (OMIM #614008). This disorder is caused by a mutation in BANF1, a gene encoding a protein with essential functions in the assembly of the nuclear envelope, further illustrating the importance of the nuclear lamina integrity for human health and providing additional support to the study of progeroid syndromes as a valuable source of information on human aging.
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De Menezes, Deborah Antunes, Amanda Ramos Caixeta, Isabella de Brito Alem Silva, Ana Luísa De Souza, Carolina Pessoa Rodrigues Ribeiro, Larissa Amorim Silva, Letícia Araújo Duarte, et al. "Síndrome Progeroide de Hutchinson-Gilford: Uma revisão integrativa / Hutchinson-Gilford Progeroid Syndrome: An Integrative Review." Brazilian Journal of Health Review 4, no. 5 (October 13, 2021): 21783–93. http://dx.doi.org/10.34119/bjhrv4n5-268.

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Giguet-Valard, Anna-Gaëlle, Astrid Monfort, Hugues Lucron, Helena Mosbah, Franck Boccara, Camille Vatier, Corinne Vigouroux, et al. "A Family with a Single LMNA Mutation Illustrates Diversity in Cardiac Phenotypes Associated with Laminopathic Progeroid Syndromes." Cardiogenetics 13, no. 4 (September 26, 2023): 135–44. http://dx.doi.org/10.3390/cardiogenetics13040013.

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The likely pathogenic variant c.407A>T p.Asp136Val of the LMNA gene has been recently described in a young woman presenting with atypical progeroid syndrome, associated with severe aortic valve stenosis. We further describe the cardiovascular involvement associated with the syndrome in her family. We identified seven members with a general presentation suggestive of progeroid syndrome. All of them presented heart conduction abnormalities: degenerative cardiac diseases such as coronary artery disease (two subjects) and aortic stenosis (three subjects) occurred in the 3rd–5th decade, and a young patient developed a severe dilated cardiomyopathy, leading to death at 15 years of age. The likely pathogenic variant was found in all the patients who consented to carry out the genetic test. This diverse family cardiologic phenotype emphasizes the complex molecular background at play in lamin-involved cardiac diseases, and the need for early and thorough cardiac evaluations in patients with laminopathic progeroid syndromes.
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Trani, Jean Philippe, Raphaël Chevalier, Leslie Caron, Claire El Yazidi, Natacha Broucqsault, Léa Toury, Morgane Thomas, et al. "Mesenchymal stem cells derived from patients with premature aging syndromes display hallmarks of physiological aging." Life Science Alliance 5, no. 12 (September 14, 2022): e202201501. http://dx.doi.org/10.26508/lsa.202201501.

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Progeroid syndromes are rare genetic diseases with most of autosomal dominant transmission, the prevalence of which is less than 1/10,000,000. These syndromes caused by mutations in the LMNA gene encoding A-type lamins belong to a group of disorders called laminopathies. Lamins are implicated in the architecture and function of the nucleus and chromatin. Patients affected with progeroid laminopathies display accelerated aging of mesenchymal stem cells (MSCs)–derived tissues associated with nuclear morphological abnormalities. To identify pathways altered in progeroid patients’ MSCs, we used induced pluripotent stem cells (hiPSCs) from patients affected with classical Hutchinson–Gilford progeria syndrome (HGPS, c.1824C>T—p.G608G), HGPS-like syndrome (HGPS-L; c.1868C>G—p.T623S) associated with farnesylated prelamin A accumulation, or atypical progeroid syndromes (APS; homozygous c.1583C> T—p.T528M; heterozygous c.1762T>C—p.C588R; compound heterozygous c.1583C>T and c.1619T>C—p.T528M and p.M540T) without progerin accumulation. By comparative analysis of the transcriptome and methylome of hiPSC-derived MSCs, we found that patient’s MSCs display specific DNA methylation patterns and modulated transcription at early stages of differentiation. We further explored selected biological processes deregulated in the presence of LMNA variants and confirmed alterations of age-related pathways during MSC differentiation. In particular, we report the presence of an altered mitochondrial pattern; an increased response to double-strand DNA damage; and telomere erosion in HGPS, HGPS-L, and APS MSCs, suggesting converging pathways, independent of progerin accumulation, but a distinct DNA methylation profile in HGPS and HGPS-L compared with APS cells.
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Martin, George M. "Genetic modulation of the senescent phenotype in Homo sapiens." Genome 31, no. 1 (January 1, 1989): 390–97. http://dx.doi.org/10.1139/g89-059.

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While it is important to search for unifying mechanisms of aging among a variety of model systems, evolutionary arguments suggest that the pathophysiological details of senescence may be, to some extent, species specific. Moreover, in species that are characterized by extensive genetic heterogeneity, such as our own, one is likely to find kindreds with both "private" and "public" markers of aging. Crude estimates of the number of loci with the potential to modulate aspects of the senescent phenotype of man suggest that thousands of genes could be involved. No single locus appears to modulate all features. Some affect predominately a single aspect ("unimodal progeroid syndromes"); familial Alzheimer's disease is discussed as a prototype. Linkage studies indicate genetic heterogeneity for autosomal dominant forms of the disease. Some loci affect multiple aspects of the phenotype ("segmental progeroid disorders"); the prototype is Werner's syndrome, an autosomal recessive. Cells from homozygotes behave like mutator strains and undergo accelerated senescence in vitro. Elucidation of the biochemical genetic basis of such abiotrophic disorders may shed light on specific aging processes in man.Key words: Homo sapiens, senescence, progeroid syndromes, Alzheimer's disease, linkage, Werner's syndrome, mutator strains.
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Graul-Neumann, L. M., K. Hoffmann, P. Robinson, and D. Horn. "Progeroide Variante eines Marfan-Syndroms." medizinische genetik 24, no. 4 (December 2012): 279–83. http://dx.doi.org/10.1007/s11825-012-0361-9.

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Dissertations / Theses on the topic "Syndrome progeroïde"

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Filho, Ricardo Di Lazzaro. "Estudo genético-clínico de pacientes com síndromes progeróides." Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/41/41136/tde-22012018-142854/.

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Algumas síndromes genéticas monogênicas apresentam fenótipos considerados progeróides, ou seja, desenvolvem precocemente características clínicas semelhantes às observadas no envelhecimento humano normal. A relação fisiopatológica entre essas doenças e o processo de envelhecimento vem sendo estudada, sendo que o entendimento dos mecanismos moleculares em um campo contribui para a compreensão do outro. As síndromes de Hutchinson-Gilford e Rothmund-Thomson são duas condições progeróides raras, já bem caracterizadas clinicamente, que são causadas por alterações nos genes LMNA (em um alelo) e RECQL4 (nos dois alelos), respectivamente. No entanto, em cerca de 40% a 60% dos indivíduos com a síndrome de Rothmund-Thomson, não são encontradas mutações em RECQL4, constituindo um subgrupo chamado de tipo I; desse modo, os casos com alteração no gene constituem o tipo II da síndrome. Indivíduos com o tipo II apresentam um risco aumentado para o desenvolvimento de câncer, particularmente o osteossarcoma. Neste trabalho, nove pacientes com sinais progeróides foram avaliados clinicamente e tiveram o DNA sequenciado. Um paciente recebeu o diagnóstico clínico de síndrome de Hutchinson-Gilford, que foi confirmado pela mutação patogênica mais frequente encontrada no gene LMNA (p.Gly608Gly). Oito pacientes jovens, com mediana de idade de 2 anos e 2 meses, foram diagnosticados clinicamente como afetados pela síndrome de Rothmund-Thomson, cujas características clínicas mais comuns incluíam déficit pôndero-estatural, cabelos e sobrancelhas/cílios esparsos, fronte ampla, lesão cutânea (eritema em face e lesão poiquilodérmica) e anomalias ósseas, alterações típicas da síndrome. Catarata estava presente em 50% dos indivíduos. Nenhum dos pacientes desenvolveu algum tipo de tumor até o momento. O sequenciamento do gene RECQL4 mostrou a presença de três variantes patogênicas diferentes, em três probandos (37,5%), sendo dois em homozigose e um em heterozigose composta, todas já descritas previamente na literatura. Em busca de alterações em outro gene que pudesse explicar o quadro apresentado pelos pacientes sem mutação, três dos probandos, incluindo os genitores de um deles, tiveram o exoma sequenciado. No entanto, não foram encontradas, nessa etapa, variantes adicionais que explicassem na totalidade os fenótipos apresentados. Comparando os achados clínicos dos pacientes com a síndrome de Rothmund-Thomson tipo I e tipo II, foi observada diferença estatisticamente significante na incidência de catarata subcapsular nos pacientes sem mutação (p<0,05), semelhante ao que é descrito na literatura. Diante dos achados clínicos e moleculares obtidos, foi realizado o aconselhamento genético para todos os indivíduos, enfatizando a evolução, os cuidados e acompanhamentos necessários para as duas doenças em questão e fornecendo informações aos genitores dos probandos sobre o risco de recorrência para a prole futura
Some monogenic disorders exhibit progeroid phenotypes, in other words, they develop premature characteristics similar to those observed in normal human aging. The physiopathological correlation between these diseases and the aging process has being studied, and the understanding of the molecular mechanisms in one field contributes to the understanding of the other. The Hutchinson-Gilford and Rothmund-Thomson syndromes are two clinically well-characterized rare progerioid conditions that are caused by changes in the LMNA (in one allele) and RECQL4 (in both alleles) genes, respectively. However, in about 40% to 60% of individuals with Rothmund-Thomson syndrome, no mutations are found in RECQL4, constituting a subgroup called type I; thus, cases with mutations in the gene constitute the type II group of the syndrome. Individuals with type II have an increased risk for the development of cancer, particularly osteosarcoma. In this study, nine patients with progerioid signs were clinically evaluated and had the DNA sequenced. One patient was clinically diagnosed with Hutchinson-Gilford syndrome, which was confirmed by the most frequent pathogenic mutation found in the LMNA gene (p.Gly608Gly). Eight young patients with median age of 2 years and 2 months were clinically diagnosed as affected by Rothmund-Thomson syndrome, whose most common clinical features included: short stature; sparse hair, eyebrows and eyelashes; erythematous skin lesions and poikiloderma; and bone abnormalities; all typical of the syndrome. Cataract was present in 50% of individuals. None of the patients has developed any type of tumor at this time. Sequencing of the RECQL4 gene showed the presence of three different pathogenic variants in three probands (37.5%), two in homozygous and one in compound heterozygosity, all previously described in the literature. In search of alterations in another gene that could explain the phenotype presented by the patients without mutation, three of the probands, including the parents of one of them, had the exoma sequenced. However, there were no additional variants at this stage that fully explained the phenotypes presented by these individuals. Comparing the clinical findings of patients with Rothmund-Thomson syndrome type I and type II, a statistically significant difference was observed in the incidence of subcapsular cataract in patients without mutation (p <0.05), similar to that described in the literature. In light of the clinical and molecular findings, genetic counseling was performed for all individuals, emphasizing the evolution, care and follow-up needed for the two diseases in question and providing information to the parents of the probands on the risk of recurrence for future offspring
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Smallwood, Dawn Teresca. "Investigating lamin A mutations in progeroid syndromes and partial lipodystrophy." Thesis, University of Leicester, 2012. http://hdl.handle.net/2381/11070.

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Lamin A/C is a component of the nuclear lamina that contributes to nuclear integrity, chromatin organisation, gene transcription and DNA replication. Mutation of the LMNA gene, encoding lamin A/C, causes a number of diseases affecting different tissues, but the mechanism(s) by which this widely expressed protein causes tissue-specific disease remains unclear. Hutchinson-Gilford progeria syndrome (HGPS) is an early-onset premature aging disorder. The most common LMNA mutation (G608G) prevents complete posttranslational processing of lamin A, resulting in aberrant retention of a farnesyl group. In this study, a cohort of children with progeroid phenotypes were screened for genetic defects. The G608G mutation was identified in one patient with a classical phenotype. A second patient with mild progeria carried a rare T623S mutation, which also results in aberrant farnesylation of lamin A. In contrast, a severe progeroid phenotype resulted from homozygous mutation of ZMPSTE24, the key enzyme in lamin A processing. Studies of skin fibroblasts showed a correlation between farnesylated lamin A level and disease severity. FRAP studies revealed that retention of the farnsesyl group causes a 50% decrease in mobility of lamin A, irrespective of the exact mutation. Interestingly, one non-farnesylated mutant also had a 50% reduction in mobility, whilst other non-farnesylated mutants had normal mobility. The results of these studies indicate that incomplete processing of lamin A is an important contributor to severity of progeroid disorders but, in agreement with other reports, is not the only disease mechanism involved. Familial partial lipodystrophy (FPLD) is a fat wasting disorder also resulting from LMNA mutations. Preliminary analysis of the adipogenic potential of mesenchymal stem cells isolated from FPLD patients do not produce detectable levels of adipogenesis. Preliminary immunofluorescence and binding studies in FPLD and progeria tend to support existing evidence that mislocalisation of the adipogenic factor SREBP1 may underlie the lipodystrophy phenotype.
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Annab, Karima. "Etude de l’expression génique de différents syndromes progéroïdes en utilisant le modèle des cellules souches à pluripotence induite." Thesis, Aix-Marseille, 2019. http://www.theses.fr/2019AIXM0101.

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Les syndromes progéroïdes regroupent un ensemble de pathologies caractérisées par un vieillissement précoce et accéléré. Le syndrome le plus connu et étudié est la progéria de Hutchinson-Gilford dont l'incidence est de 1 cas sur 8 millions ce qui en fait une maladie très rare. Nous avons étudié trois symptômes progéroïdes dont le syndrome HGPS, un syndrome HGPS-like ainsi qu'un syndrome APS. Ces pathologies ont de nombreux symptômes en commun dont une ostéolyse, une lipodystrophie, ainsi qu'une atteinte cardiovasculaire. Ces trois syndromes sont provoqués par différentes mutations du gène LMNA qui code pour les Lamines A et C. Nous avons utilisé le modèle des iPSCs afin d'étudier in vitro la physiopathologie de ces trois syndromes en les comparant à des cellules contrôles. Les cellules dérivées de la voie mésenchymateuse étant majoritairement altérées dans ces pathologies, nous avons créé des modèles in vitro d'étude de la différentiation en MSCs. De plus, ces patients présentant des altérations arterio-veineuses, nous avons analysé la différenciation en VSMCs. Le phénotype des ces cellules a été analysé et les profils transcriptomiques comparés pour les différentes lignées. Des gènes communs, impliqués dans le stress oxydatif et dans des systèmes de réparation géniques ont été retrouvés comme étant altérés. De plus, nous avons mis en évidence des altérations de voies de signalisation indispensables à la survie et à la prolifération cellulaire en comparant les cellules progéroïdes aux contrôles. Certaines de ces voies biologiques ouvrent de nouvelles perspectives dans la compréhension des symptômes observés chez ces patients
Progeroid syndromes are a group of pathologies characterized by accelerated and early aging. One of the most studied of these diseases is HGPS, with an estimated incidence of 1 in 8 millions birth making it an extremely rare disease. We focused our attention on three different progeroid syndromes including classic HGPS, a HGPS-like and an atypical progeroid syndrome. These pathologies share many symptoms, including osteolysis, lipodystrophy, and cardiovascular alterations. These 3 syndromes are caused by 3 different mutations in the LMNA gene that encodes A- and C-type lamins, inducing production of a truncated Lamin A in HGPS and HGPS-like and production of a mutated Lamin with a p.T528M substitution in APS. We produced hiPSCs to create a model of these different diseases and investigate in vitro the physiopathology of these syndromes by comparing them to control cells. Cells derived from mesenchymal stem cells being the most impaired type of tissue, we established in vitro models in order to study the differentiation of hiPSCs into MSCs. In addition given the massive cardiovascular defects in these patients, we also investigated differentiation toward the VSMCs. Cell phenotypes were carefully characterized and we compared the transcripttomic profile of the different cell types. We identified dysregulation in genes involved in oxidative stress response and in DNA repair in progeroid cells. In addition, pathways essential for cell survival and proliferation are also modified when comparing progeroid and controls cells. Altogether, these results might explain some of the symptoms observed in progeroid patients but also reveal pathways involved in ageing
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Eisch, Veronika [Verfasser], Karima [Akademischer Betreuer] Djabali, Bertold [Gutachter] Hock, and Karima [Gutachter] Djabali. "Characterizing the spatiotemporal distribution and interaction of the lamin A isoforms progerin and prelamin A during mitosis in the Progeroid Syndromes Hutchinson-Gilford progeria syndrome and Mandibuloacral Dysplasia Type B / Veronika Eisch ; Gutachter: Bertold Hock, Karima Djabali ; Betreuer: Karima Djabali." München : Universitätsbibliothek der TU München, 2020. http://d-nb.info/1227580355/34.

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Turotszy, Alicja. "The role of NARF and other novel progeria-associated genes/proteins in ageing processes." Doctoral thesis, 2020. http://hdl.handle.net/21.11130/00-1735-0000-0005-155F-A.

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Book chapters on the topic "Syndrome progeroïde"

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Huang, Shurong, Brian K. Kennedy, and Junko Oshima. "LMNA Mutations in Progeroid Syndromes." In Nuclear Organization in Development and Disease, 197–207. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/0470093765.ch13.

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Agrelo, Ruben. "Epigenetic Silencing of Progeroid Syndromes." In Epigenetics of Aging, 345–69. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-0639-7_19.

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Pascual-Castroviejo, Ignacio, and Martino Ruggieri. "Progeria and Progeroid Syndromes (Premature Ageing Disorders)." In Neurocutaneous Disorders Phakomatoses and Hamartoneoplastic Syndromes, 847–78. Vienna: Springer Vienna, 2008. http://dx.doi.org/10.1007/978-3-211-69500-5_54.

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Martin, George M. "Keynote Address: Genetics and Aging; The Werner Syndrome as a Segmental Progeroid Syndrome." In Advances in Experimental Medicine and Biology, 161–70. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-7853-2_5.

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Davis, Terence. "Progeroid Syndromes: Role of Accelerated Fibroblast Senescence and p38 Activation." In Tumor Dormancy, Quiescence, and Senescence, Vol. 3, 25–39. Dordrecht: Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-017-9325-4_3.

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Fechtner, Lisa, and Thorsten Pfirrmann. "Ubiquitin Ligases Involved in Progeroid Syndromes and Age-Associated Pathologies." In Proteostasis and Proteolysis, 81–94. Boca Raton: CRC Press, 2021. http://dx.doi.org/10.1201/9781003048138-07.

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"Progeroid Syndromes." In Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 1562. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_13497.

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"Epigenetic Silencing of Progeroid Syndromes." In Epigenetics of Aging, E1. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-0639-7_26.

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"Cockayne Syndrome: Its Overlap with Xeroderm a Pigmentosum and Other Progeroid Syndromes." In Molecular Mechanisms of Cockayne Syndrome, 99–108. CRC Press, 2009. http://dx.doi.org/10.1201/9781498712705-13.

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Kresse, Hans. "Chapter 9 Progeroid form of Ehlers-Danlos syndrome." In New Comprehensive Biochemistry, 331–36. Elsevier, 1996. http://dx.doi.org/10.1016/s0167-7306(08)60295-1.

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Conference papers on the topic "Syndrome progeroïde"

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Hartge, D., M. Gembicki, and J. Weichert. "Angebornenes progeroides Syndrom aka Wiedemann-Rautenstrauch-Syndrom (WRS) – Eine seltene Ursache einer fetalen Wachstumsrestriktion." In Interdisziplinärer Kongress | Ultraschall 2018 – 42. Dreiländertreffen SGUM | DEGUM | ÖGUM. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1670389.

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You might also be interested in the extended bibliographies on the topic 'Syndrome progeroïde' for particular source types:
Journal articles
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