Advanced Search
Display options
Filter resources
Text Availability
Article type
Publication date
Species
Language
Sex
Age
Showing 1 to 12 of 13 entries
Sorted by: Best Match Show Resources per page
Pathological relationships involving iron and myelin may constitute a shared mechanism linking various rare and common brain diseases.

Rare diseases (Austin, Tex.)

Heidari M, Gerami SH, Bassett B, Graham RM, Chua AC, Aryal R, House MJ, Collingwood JF, Bettencourt C, Houlden H, Ryten M, Olynyk JK, Trinder D, Johnstone DM, Milward EA.
PMID: 27500074
Rare Dis. 2016 Jun 22;4(1):e1198458. doi: 10.1080/21675511.2016.1198458. eCollection 2016.

We previously demonstrated elevated brain iron levels in myelinated structures and associated cells in a hemochromatosis Hfe (-/-) xTfr2 (mut) mouse model. This was accompanied by altered expression of a group of myelin-related genes, including a suite of genes...

Cite
Heidari M, Gerami SH, Bassett B, et al. Pathological relationships involving iron and myelin may constitute a shared mechanism linking various rare and common brain diseases. Rare Dis. 2016;4(1):e1198458doi: 10.1080/21675511.2016.1198458.
Heidari, M., Gerami, S. H., Bassett, B., Graham, R. M., Chua, A. C., Aryal, R., House, M. J., Collingwood, J. F., Bettencourt, C., Houlden, H., Ryten, M., Olynyk, J. K., Trinder, D., Johnstone, D. M., & Milward, E. A. (2016). Pathological relationships involving iron and myelin may constitute a shared mechanism linking various rare and common brain diseases. Rare diseases (Austin, Tex.), 4(1), e1198458. https://doi.org/10.1080/21675511.2016.1198458
Heidari, Moones, et al. "Pathological relationships involving iron and myelin may constitute a shared mechanism linking various rare and common brain diseases." Rare diseases (Austin, Tex.) vol. 4,1 (2016): e1198458. doi: https://doi.org/10.1080/21675511.2016.1198458
Heidari M, Gerami SH, Bassett B, Graham RM, Chua AC, Aryal R, House MJ, Collingwood JF, Bettencourt C, Houlden H, Ryten M, Olynyk JK, Trinder D, Johnstone DM, Milward EA. Pathological relationships involving iron and myelin may constitute a shared mechanism linking various rare and common brain diseases. Rare Dis. 2016 Jun 22;4(1):e1198458. doi: 10.1080/21675511.2016.1198458. eCollection 2016. PMID: 27500074; PMCID: PMC4961263.
Copy Download .nbib Format: NLM
Genomics implicates adaptive and innate immunity in Alzheimer's and Parkinson's diseases.

Annals of clinical and translational neurology

Gagliano SA, Pouget JG, Hardy J, Knight J, Barnes MR, Ryten M, Weale ME.
PMID: 28097204
Ann Clin Transl Neurol. 2016 Nov 04;3(12):924-933. doi: 10.1002/acn3.369. eCollection 2016 Dec.

OBJECTIVES: We assessed the current genetic evidence for the involvement of various cell types and tissue types in the etiology of neurodegenerative diseases, especially in relation to the neuroinflammatory hypothesis of neurodegenerative diseases.METHODS: We obtained large-scale genome-wide association study...

Cite
Gagliano SA, Pouget JG, Hardy J, et al. Genomics implicates adaptive and innate immunity in Alzheimer's and Parkinson's diseases. Ann Clin Transl Neurol. 2016;3(12):924-933doi: 10.1002/acn3.369.
Gagliano, S. A., Pouget, J. G., Hardy, J., Knight, J., Barnes, M. R., Ryten, M., & Weale, M. E. (2016). Genomics implicates adaptive and innate immunity in Alzheimer's and Parkinson's diseases. Annals of clinical and translational neurology, 3(12), 924-933. https://doi.org/10.1002/acn3.369
Gagliano, Sarah A, et al. "Genomics implicates adaptive and innate immunity in Alzheimer's and Parkinson's diseases." Annals of clinical and translational neurology vol. 3,12 (2016): 924-933. doi: https://doi.org/10.1002/acn3.369
Gagliano SA, Pouget JG, Hardy J, Knight J, Barnes MR, Ryten M, Weale ME. Genomics implicates adaptive and innate immunity in Alzheimer's and Parkinson's diseases. Ann Clin Transl Neurol. 2016 Nov 04;3(12):924-933. doi: 10.1002/acn3.369. eCollection 2016 Dec. PMID: 28097204; PMCID: PMC5224821.
Copy Download .nbib Format: NLM
Moving beyond neurons: the role of cell type-specific gene regulation in Parkinson's disease heritability.

NPJ Parkinson's disease

Reynolds RH, Botía J, Nalls MA, Hardy J, Gagliano Taliun SA, Ryten M.
PMID: 31016231
NPJ Parkinsons Dis. 2019 Apr 17;5:6. doi: 10.1038/s41531-019-0076-6. eCollection 2019.

Parkinson's disease (PD), with its characteristic loss of nigrostriatal dopaminergic neurons and deposition of α-synuclein in neurons, is often considered a neuronal disorder. However, in recent years substantial evidence has emerged to implicate glial cell types, such as astrocytes...

Cite
Reynolds RH, Botía J, Nalls MA. Moving beyond neurons: the role of cell type-specific gene regulation in Parkinson's disease heritability. NPJ Parkinsons Dis. 2019;5:6doi: 10.1038/s41531-019-0076-6.
Reynolds, R. H., Botía, J., Nalls, M. A., Hardy, J., Gagliano Taliun, S. A., & Ryten, M. (2019). Moving beyond neurons: the role of cell type-specific gene regulation in Parkinson's disease heritability. NPJ Parkinson's disease, 56. https://doi.org/10.1038/s41531-019-0076-6
Reynolds, Regina H, et al. "Moving beyond neurons: the role of cell type-specific gene regulation in Parkinson's disease heritability." NPJ Parkinson's disease vol. 5 (2019): 6. doi: https://doi.org/10.1038/s41531-019-0076-6
Reynolds RH, Botía J, Nalls MA, Hardy J, Gagliano Taliun SA, Ryten M. Moving beyond neurons: the role of cell type-specific gene regulation in Parkinson's disease heritability. NPJ Parkinsons Dis. 2019 Apr 17;5:6. doi: 10.1038/s41531-019-0076-6. eCollection 2019. PMID: 31016231; PMCID: PMC6470136.
Copy Download .nbib Format: NLM
Identification of Candidate Parkinson Disease Genes by Integrating Genome-Wide Association Study, Expression, and Epigenetic Data Sets.

JAMA neurology

Kia DA, Zhang D, Guelfi S, Manzoni C, Hubbard L, Reynolds RH, Botía J, Ryten M, Ferrari R, Lewis PA, Williams N, Trabzuni D, Hardy J, Wood NW.
PMID: 33523105
JAMA Neurol. 2021 Apr 01;78(4):464-472. doi: 10.1001/jamaneurol.2020.5257.

IMPORTANCE: Substantial genome-wide association study (GWAS) work in Parkinson disease (PD) has led to the discovery of an increasing number of loci shown reliably to be associated with increased risk of disease. Improved understanding of the underlying genes and...

Cite
Kia DA, Zhang D, Guelfi S, et al. Identification of Candidate Parkinson Disease Genes by Integrating Genome-Wide Association Study, Expression, and Epigenetic Data Sets. JAMA Neurol. 2021;78(4):464-472doi: 10.1001/jamaneurol.2020.5257.
Kia, D. A., Zhang, D., Guelfi, S., Manzoni, C., Hubbard, L., Reynolds, R. H., Botía, J., Ryten, M., Ferrari, R., Lewis, P. A., Williams, N., Trabzuni, D., Hardy, J., Wood, N. W. (2021). Identification of Candidate Parkinson Disease Genes by Integrating Genome-Wide Association Study, Expression, and Epigenetic Data Sets. JAMA neurology, 78(4), 464-472. https://doi.org/10.1001/jamaneurol.2020.5257
Kia, Demis A, et al. "Identification of Candidate Parkinson Disease Genes by Integrating Genome-Wide Association Study, Expression, and Epigenetic Data Sets." JAMA neurology vol. 78,4 (2021): 464-472. doi: https://doi.org/10.1001/jamaneurol.2020.5257
Kia DA, Zhang D, Guelfi S, Manzoni C, Hubbard L, Reynolds RH, Botía J, Ryten M, Ferrari R, Lewis PA, Williams N, Trabzuni D, Hardy J, Wood NW. Identification of Candidate Parkinson Disease Genes by Integrating Genome-Wide Association Study, Expression, and Epigenetic Data Sets. JAMA Neurol. 2021 Apr 01;78(4):464-472. doi: 10.1001/jamaneurol.2020.5257. PMID: 33523105; PMCID: PMC7851759.
Copy Download .nbib Format: NLM
Identification of Candidate Parkinson Disease Genes by Integrating Genome-Wide Association Study, Expression, and Epigenetic Data Sets.

JAMA neurology

Kia DA, Zhang D, Guelfi S, Manzoni C, Hubbard L, Reynolds RH, Botía J, Ryten M, Ferrari R, Lewis PA, Williams N, Trabzuni D, Hardy J, Wood NW.
PMID: 33523105
JAMA Neurol. 2021 Apr 01;78(4):464-472. doi: 10.1001/jamaneurol.2020.5257.

IMPORTANCE: Substantial genome-wide association study (GWAS) work in Parkinson disease (PD) has led to the discovery of an increasing number of loci shown reliably to be associated with increased risk of disease. Improved understanding of the underlying genes and...

Cite
Kia DA, Zhang D, Guelfi S, et al. Identification of Candidate Parkinson Disease Genes by Integrating Genome-Wide Association Study, Expression, and Epigenetic Data Sets. JAMA Neurol. 2021;78(4):464-472doi: 10.1001/jamaneurol.2020.5257.
Kia, D. A., Zhang, D., Guelfi, S., Manzoni, C., Hubbard, L., Reynolds, R. H., Botía, J., Ryten, M., Ferrari, R., Lewis, P. A., Williams, N., Trabzuni, D., Hardy, J., Wood, N. W. (2021). Identification of Candidate Parkinson Disease Genes by Integrating Genome-Wide Association Study, Expression, and Epigenetic Data Sets. JAMA neurology, 78(4), 464-472. https://doi.org/10.1001/jamaneurol.2020.5257
Kia, Demis A, et al. "Identification of Candidate Parkinson Disease Genes by Integrating Genome-Wide Association Study, Expression, and Epigenetic Data Sets." JAMA neurology vol. 78,4 (2021): 464-472. doi: https://doi.org/10.1001/jamaneurol.2020.5257
Kia DA, Zhang D, Guelfi S, Manzoni C, Hubbard L, Reynolds RH, Botía J, Ryten M, Ferrari R, Lewis PA, Williams N, Trabzuni D, Hardy J, Wood NW. Identification of Candidate Parkinson Disease Genes by Integrating Genome-Wide Association Study, Expression, and Epigenetic Data Sets. JAMA Neurol. 2021 Apr 01;78(4):464-472. doi: 10.1001/jamaneurol.2020.5257. PMID: 33523105; PMCID: PMC7851759.
Copy Download .nbib Format: NLM
Incomplete annotation has a disproportionate impact on our understanding of Mendelian and complex neurogenetic disorders.

Science advances

Zhang D, Guelfi S, Garcia-Ruiz S, Costa B, Reynolds RH, D'Sa K, Liu W, Courtin T, Peterson A, Jaffe AE, Hardy J, Botía JA, Collado-Torres L, Ryten M.
PMID: 32917675
Sci Adv. 2020 Jun 10;6(24). doi: 10.1126/sciadv.aay8299. Print 2020 Jun.

Growing evidence suggests that human gene annotation remains incomplete; however, it is unclear how this affects different tissues and our understanding of different disorders. Here, we detect previously unannotated transcription from Genotype-Tissue Expression RNA sequencing data across 41 human...

Cite
Zhang D, Guelfi S, Garcia-Ruiz S, et al. Incomplete annotation has a disproportionate impact on our understanding of Mendelian and complex neurogenetic disorders. Sci Adv. 2020;6(24)doi: 10.1126/sciadv.aay8299.
Zhang, D., Guelfi, S., Garcia-Ruiz, S., Costa, B., Reynolds, R. H., D'Sa, K., Liu, W., Courtin, T., Peterson, A., Jaffe, A. E., Hardy, J., Botía, J. A., Collado-Torres, L., & Ryten, M. (2020). Incomplete annotation has a disproportionate impact on our understanding of Mendelian and complex neurogenetic disorders. Science advances, 6(24), . https://doi.org/10.1126/sciadv.aay8299
Zhang, David, et al. "Incomplete annotation has a disproportionate impact on our understanding of Mendelian and complex neurogenetic disorders." Science advances vol. 6,24 (2020). doi: https://doi.org/10.1126/sciadv.aay8299
Zhang D, Guelfi S, Garcia-Ruiz S, Costa B, Reynolds RH, D'Sa K, Liu W, Courtin T, Peterson A, Jaffe AE, Hardy J, Botía JA, Collado-Torres L, Ryten M. Incomplete annotation has a disproportionate impact on our understanding of Mendelian and complex neurogenetic disorders. Sci Adv. 2020 Jun 10;6(24). doi: 10.1126/sciadv.aay8299. Print 2020 Jun. PMID: 32917675; PMCID: PMC7286675.
Copy Download .nbib Format: NLM
Analysis of brain atrophy and local gene expression in genetic frontotemporal dementia.

Brain communications

Altmann A, Cash DM, Bocchetta M, Heller C, Reynolds R, Moore K, Convery RS, Thomas DL, van Swieten JC, Moreno F, Sanchez-Valle R, Borroni B, Laforce R, Masellis M, Tartaglia MC, Graff C, Galimberti D, Rowe JB, Finger E, Synofzik M, Vandenberghe R, de Mendonça A, Tagliavini F, Santana I, Ducharme S, Butler CR, Gerhard A, Levin J, Danek A, Frisoni G, Ghidoni R, Sorbi S, Otto M, Ryten M, Rohrer JD.
PMID: 33210084
Brain Commun. 2020 Aug 19;2(2). doi: 10.1093/braincomms/fcaa122. eCollection 2020 Jul.

Frontotemporal dementia is a heterogeneous neurodegenerative disorder characterized by neuronal loss in the frontal and temporal lobes. Despite progress in understanding which genes are associated with the aetiology of frontotemporal dementia, the biological basis of how mutations in these...

Cite
Altmann A, Cash DM, Bocchetta M, et al. Analysis of brain atrophy and local gene expression in genetic frontotemporal dementia. Brain Commun. 2020;2(2)doi: 10.1093/braincomms/fcaa122.
Altmann, A., Cash, D. M., Bocchetta, M., Heller, C., Reynolds, R., Moore, K., Convery, R. S., Thomas, D. L., van Swieten, J. C., Moreno, F., Sanchez-Valle, R., Borroni, B., Laforce, R., Masellis, M., Tartaglia, M. C., Graff, C., Galimberti, D., Rowe, J. B., Finger, E., Synofzik, M., Vandenberghe, R., de Mendonça, A., Tagliavini, F., Santana, I., Ducharme, S., Butler, C. R., Gerhard, A., Levin, J., Danek, A., Frisoni, G., Ghidoni, R., Sorbi, S., Otto, M., Ryten, M., Rohrer, J. D. (2020). Analysis of brain atrophy and local gene expression in genetic frontotemporal dementia. Brain communications, 2(2), . https://doi.org/10.1093/braincomms/fcaa122
Altmann, Andre, et al. "Analysis of brain atrophy and local gene expression in genetic frontotemporal dementia." Brain communications vol. 2,2 (2020). doi: https://doi.org/10.1093/braincomms/fcaa122
Altmann A, Cash DM, Bocchetta M, Heller C, Reynolds R, Moore K, Convery RS, Thomas DL, van Swieten JC, Moreno F, Sanchez-Valle R, Borroni B, Laforce R, Masellis M, Tartaglia MC, Graff C, Galimberti D, Rowe JB, Finger E, Synofzik M, Vandenberghe R, de Mendonça A, Tagliavini F, Santana I, Ducharme S, Butler CR, Gerhard A, Levin J, Danek A, Frisoni G, Ghidoni R, Sorbi S, Otto M, Ryten M, Rohrer JD. Analysis of brain atrophy and local gene expression in genetic frontotemporal dementia. Brain Commun. 2020 Aug 19;2(2). doi: 10.1093/braincomms/fcaa122. eCollection 2020 Jul. PMID: 33210084; PMCID: PMC7667525.
Copy Download .nbib Format: NLM
Cross-platform transcriptional profiling identifies common and distinct molecular pathologies in Lewy body diseases.

Acta neuropathologica

Feleke R, Reynolds RH, Smith AM, Tilley B, Taliun SAG, Hardy J, Matthews PM, Gentleman S, Owen DR, Johnson MR, Srivastava PK, Ryten M.
PMID: 34309761
Acta Neuropathol. 2021 Sep;142(3):449-474. doi: 10.1007/s00401-021-02343-x. Epub 2021 Jul 26.

Parkinson's disease (PD), Parkinson's disease with dementia (PDD) and dementia with Lewy bodies (DLB) are three clinically, genetically and neuropathologically overlapping neurodegenerative diseases collectively known as the Lewy body diseases (LBDs). A variety of molecular mechanisms have been implicated...

Cite
Feleke R, Reynolds RH, Smith AM, et al. Cross-platform transcriptional profiling identifies common and distinct molecular pathologies in Lewy body diseases. Acta Neuropathol. 2021;142(3):449-474doi: 10.1007/s00401-021-02343-x.
Feleke, R., Reynolds, R. H., Smith, A. M., Tilley, B., Taliun, S. A. G., Hardy, J., Matthews, P. M., Gentleman, S., Owen, D. R., Johnson, M. R., Srivastava, P. K., & Ryten, M. (2021). Cross-platform transcriptional profiling identifies common and distinct molecular pathologies in Lewy body diseases. Acta neuropathologica, 142(3), 449-474. https://doi.org/10.1007/s00401-021-02343-x
Feleke, Rahel, et al. "Cross-platform transcriptional profiling identifies common and distinct molecular pathologies in Lewy body diseases." Acta neuropathologica vol. 142,3 (2021): 449-474. doi: https://doi.org/10.1007/s00401-021-02343-x
Feleke R, Reynolds RH, Smith AM, Tilley B, Taliun SAG, Hardy J, Matthews PM, Gentleman S, Owen DR, Johnson MR, Srivastava PK, Ryten M. Cross-platform transcriptional profiling identifies common and distinct molecular pathologies in Lewy body diseases. Acta Neuropathol. 2021 Sep;142(3):449-474. doi: 10.1007/s00401-021-02343-x. Epub 2021 Jul 26. PMID: 34309761; PMCID: PMC8357687.
Copy Download .nbib Format: NLM
Mitochondria function associated genes contribute to Parkinson's Disease risk and later age at onset.

NPJ Parkinson's disease

Billingsley KJ, Barbosa IA, Bandrés-Ciga S, Quinn JP, Bubb VJ, Deshpande C, Botia JA, Reynolds RH, Zhang D, Simpson MA, Blauwendraat C, Gan-Or Z, Gibbs JR, Nalls MA, Singleton A, Ryten M, Koks S.
PMID: 31123700
NPJ Parkinsons Dis. 2019 May 22;5:8. doi: 10.1038/s41531-019-0080-x. eCollection 2019.

Mitochondrial dysfunction has been implicated in the etiology of monogenic Parkinson's disease (PD). Yet the role that mitochondrial processes play in the most common form of the disease; sporadic PD, is yet to be fully established. Here, we comprehensively...

Cite
Billingsley KJ, Barbosa IA, Bandrés-Ciga S, et al. Mitochondria function associated genes contribute to Parkinson's Disease risk and later age at onset. NPJ Parkinsons Dis. 2019;5:8doi: 10.1038/s41531-019-0080-x.
Billingsley, K. J., Barbosa, I. A., Bandrés-Ciga, S., Quinn, J. P., Bubb, V. J., Deshpande, C., Botia, J. A., Reynolds, R. H., Zhang, D., Simpson, M. A., Blauwendraat, C., Gan-Or, Z., Gibbs, J. R., Nalls, M. A., Singleton, A., Ryten, M., & Koks, S. (2019). Mitochondria function associated genes contribute to Parkinson's Disease risk and later age at onset. NPJ Parkinson's disease, 58. https://doi.org/10.1038/s41531-019-0080-x
Billingsley, Kimberley J, et al. "Mitochondria function associated genes contribute to Parkinson's Disease risk and later age at onset." NPJ Parkinson's disease vol. 5 (2019): 8. doi: https://doi.org/10.1038/s41531-019-0080-x
Billingsley KJ, Barbosa IA, Bandrés-Ciga S, Quinn JP, Bubb VJ, Deshpande C, Botia JA, Reynolds RH, Zhang D, Simpson MA, Blauwendraat C, Gan-Or Z, Gibbs JR, Nalls MA, Singleton A, Ryten M, Koks S. Mitochondria function associated genes contribute to Parkinson's Disease risk and later age at onset. NPJ Parkinsons Dis. 2019 May 22;5:8. doi: 10.1038/s41531-019-0080-x. eCollection 2019. PMID: 31123700; PMCID: PMC6531455.
Copy Download .nbib Format: NLM
Correction to: Picomolar concentrations of oligomeric alpha-synuclein sensitizes TLR4 to play an initiating role in Parkinson's disease pathogenesis.

Acta neuropathologica

Hughes CD, Choi ML, Ryten M, Hopkins L, Drews A, Botía JA, Iljina M, Rodrigues M, Gagliano SA, Gandhi S, Bryant C, Klenerman D.
PMID: 30328509
Acta Neuropathol. 2019 Jan;137(1):121. doi: 10.1007/s00401-018-1919-7.

In the original publication of this article, the author Magarida Rodrigues was written incorrectly.

Cite
Hughes CD, Choi ML, Ryten M, et al. Correction to: Picomolar concentrations of oligomeric alpha-synuclein sensitizes TLR4 to play an initiating role in Parkinson's disease pathogenesis. Acta Neuropathol. 2019;137(1):121doi: 10.1007/s00401-018-1919-7.
Hughes, C. D., Choi, M. L., Ryten, M., Hopkins, L., Drews, A., Botía, J. A., Iljina, M., Rodrigues, M., Gagliano, S. A., Gandhi, S., Bryant, C., & Klenerman, D. (2019). Correction to: Picomolar concentrations of oligomeric alpha-synuclein sensitizes TLR4 to play an initiating role in Parkinson's disease pathogenesis. Acta neuropathologica, 137(1), 121. https://doi.org/10.1007/s00401-018-1919-7
Hughes, Craig D, et al. "Correction to: Picomolar concentrations of oligomeric alpha-synuclein sensitizes TLR4 to play an initiating role in Parkinson's disease pathogenesis." Acta neuropathologica vol. 137,1 (2019): 121. doi: https://doi.org/10.1007/s00401-018-1919-7
Hughes CD, Choi ML, Ryten M, Hopkins L, Drews A, Botía JA, Iljina M, Rodrigues M, Gagliano SA, Gandhi S, Bryant C, Klenerman D. Correction to: Picomolar concentrations of oligomeric alpha-synuclein sensitizes TLR4 to play an initiating role in Parkinson's disease pathogenesis. Acta Neuropathol. 2019 Jan;137(1):121. doi: 10.1007/s00401-018-1919-7. PMID: 30328509; PMCID: PMC6828357.
Copy Download .nbib Format: NLM
Genetic analysis of amyotrophic lateral sclerosis identifies contributing pathways and cell types.

Science advances

Saez-Atienzar S, Bandres-Ciga S, Langston RG, Kim JJ, Choi SW, Reynolds RH, Abramzon Y, Dewan R, Ahmed S, Landers JE, Chia R, Ryten M, Cookson MR, Nalls MA, Chiò A, Traynor BJ.
PMID: 33523907
Sci Adv. 2021 Jan 15;7(3). doi: 10.1126/sciadv.abd9036. Print 2021 Jan.

Despite the considerable progress in unraveling the genetic causes of amyotrophic lateral sclerosis (ALS), we do not fully understand the molecular mechanisms underlying the disease. We analyzed genome-wide data involving 78,500 individuals using a polygenic risk score approach to...

Cite
Saez-Atienzar S, Bandres-Ciga S, Langston RG, et al. Genetic analysis of amyotrophic lateral sclerosis identifies contributing pathways and cell types. Sci Adv. 2021;7(3)doi: 10.1126/sciadv.abd9036.
Saez-Atienzar, S., Bandres-Ciga, S., Langston, R. G., Kim, J. J., Choi, S. W., Reynolds, R. H., Abramzon, Y., Dewan, R., Ahmed, S., Landers, J. E., Chia, R., Ryten, M., Cookson, M. R., Nalls, M. A., Chiò, A., & Traynor, B. J. (2021). Genetic analysis of amyotrophic lateral sclerosis identifies contributing pathways and cell types. Science advances, 7(3), . https://doi.org/10.1126/sciadv.abd9036
Saez-Atienzar, Sara, et al. "Genetic analysis of amyotrophic lateral sclerosis identifies contributing pathways and cell types." Science advances vol. 7,3 (2021). doi: https://doi.org/10.1126/sciadv.abd9036
Saez-Atienzar S, Bandres-Ciga S, Langston RG, Kim JJ, Choi SW, Reynolds RH, Abramzon Y, Dewan R, Ahmed S, Landers JE, Chia R, Ryten M, Cookson MR, Nalls MA, Chiò A, Traynor BJ. Genetic analysis of amyotrophic lateral sclerosis identifies contributing pathways and cell types. Sci Adv. 2021 Jan 15;7(3). doi: 10.1126/sciadv.abd9036. Print 2021 Jan. PMID: 33523907; PMCID: PMC7810371.
Copy Download .nbib Format: NLM
An integrated genomic approach to dissect the genetic landscape regulating the cell-to-cell transfer of α-synuclein.

Cell reports

Kara E, Crimi A, Wiedmer A, Emmenegger M, Manzoni C, Bandres-Ciga S, D'Sa K, Reynolds RH, Botía JA, Losa M, Lysenko V, Carta M, Heinzer D, Avar M, Chincisan A, Blauwendraat C, García-Ruiz S, Pease D, Mottier L, Carrella A, Beck-Schneider D, Magalhães AD, Aemisegger C, Theocharides APA, Fan Z, Marks JD, Hopp SC, Abramov AY, Lewis PA, Ryten M, Hardy J, Hyman BT, Aguzzi A.
PMID: 34107263
Cell Rep. 2021 Jun 08;35(10):109189. doi: 10.1016/j.celrep.2021.109189.

Neuropathological and experimental evidence suggests that the cell-to-cell transfer of α-synuclein has an important role in the pathogenesis of Parkinson's disease (PD). However, the mechanism underlying this phenomenon is not fully understood. We undertook a small interfering RNA (siRNA),...

Cite
Kara E, Crimi A, Wiedmer A, et al. An integrated genomic approach to dissect the genetic landscape regulating the cell-to-cell transfer of α-synuclein. Cell Rep. 2021;35(10):109189doi: 10.1016/j.celrep.2021.109189.
Kara, E., Crimi, A., Wiedmer, A., Emmenegger, M., Manzoni, C., Bandres-Ciga, S., D'Sa, K., Reynolds, R. H., Botía, J. A., Losa, M., Lysenko, V., Carta, M., Heinzer, D., Avar, M., Chincisan, A., Blauwendraat, C., García-Ruiz, S., Pease, D., Mottier, L., Carrella, A., Beck-Schneider, D., Magalhães, A. D., Aemisegger, C., Theocharides, A. P. A., Fan, Z., Marks, J. D., Hopp, S. C., Abramov, A. Y., Lewis, P. A., Ryten, M., Hardy, J., Hyman, B. T., & Aguzzi, A. (2021). An integrated genomic approach to dissect the genetic landscape regulating the cell-to-cell transfer of α-synuclein. Cell reports, 35(10), 109189. https://doi.org/10.1016/j.celrep.2021.109189
Kara, Eleanna, et al. "An integrated genomic approach to dissect the genetic landscape regulating the cell-to-cell transfer of α-synuclein." Cell reports vol. 35,10 (2021): 109189. doi: https://doi.org/10.1016/j.celrep.2021.109189
Kara E, Crimi A, Wiedmer A, Emmenegger M, Manzoni C, Bandres-Ciga S, D'Sa K, Reynolds RH, Botía JA, Losa M, Lysenko V, Carta M, Heinzer D, Avar M, Chincisan A, Blauwendraat C, García-Ruiz S, Pease D, Mottier L, Carrella A, Beck-Schneider D, Magalhães AD, Aemisegger C, Theocharides APA, Fan Z, Marks JD, Hopp SC, Abramov AY, Lewis PA, Ryten M, Hardy J, Hyman BT, Aguzzi A. An integrated genomic approach to dissect the genetic landscape regulating the cell-to-cell transfer of α-synuclein. Cell Rep. 2021 Jun 08;35(10):109189. doi: 10.1016/j.celrep.2021.109189. PMID: 34107263; PMCID: PMC8207177.
Copy Download .nbib Format: NLM
Showing 1 to 12 of 13 entries