Zobrazeno 1 - 10
of 12
pro vyhledávání: '"Nima N. Naseri"'
Autor:
Ying Xue Xie, Nima N. Naseri, Jasmine Fels, Parinati Kharel, Yoonmi Na, Diane Lane, Jacqueline Burré, Manu Sharma
Publikováno v:
Nature Communications, Vol 13, Iss 1, Pp 1-16 (2022)
Release of α-synuclein aggregates by neurons instigates spread of pathology in synucleinopathies, but the mechanism remains unclear. Here the authors show that neuronally generated α-synuclein aggregates accumulate within neuronal lysosomes and are
Externí odkaz:
https://doaj.org/article/bb879c277162488aa71514ea44aa89e5
Autor:
Nima N Naseri, Joseph Bonica, Hui Xu, Larry C Park, Jamshid Arjomand, Zhengming Chen, Gary E Gibson
Publikováno v:
PLoS ONE, Vol 11, Iss 9, p e0160384 (2016)
Metabolic dysfunction is well-documented in Huntington's disease (HD). However, the link between the mutant huntingtin (mHTT) gene and the pathology is unknown. The tricarboxylic acid (TCA) cycle is the main metabolic pathway for the production of NA
Externí odkaz:
https://doaj.org/article/55ce99018e394d29bc1b712d904d5c15
Publikováno v:
Clin Genet
The neuronal ceroid lipofuscinoses (NCLs) are at least 13 distinct progressive neurodegenerative disorders unified by the accumulation of lysosomal auto-fluorescent material called lipofuscin. The only form that occurs via autosomal-dominant inherita
Autor:
Parinati Kharel, Jacqueline Burré, Milen Velinov, Nima N. Naseri, Manu Sharma, Natalia Dolzhanskaya, Rong Huang, Burce Ergel, Qingqiu Huang, Yoonmi Na
Publikováno v:
Nature structural & molecular biology
Point mutations in cysteine string protein-α (CSPα) cause dominantly inherited adult-onset neuronal ceroid lipofuscinosis (ANCL), a rapidly progressing and lethal neurodegenerative disease with no treatment. ANCL mutations are proposed to trigger C
Alzheimer's disease (AD) is characterized by two major pathological lesions in the brain, amyloid plaques and neurofibrillary tangles (NFTs) composed mainly of amyloid-β (Aβ) peptides and hyperphosphorylated tau, respectively. Although accumulation
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::e8231009bf1fc48423a00b5e3766d657
https://europepmc.org/articles/PMC7060758/
https://europepmc.org/articles/PMC7060758/
Autor:
Etty Cortes, Gary E. Gibson, Jamshid Arjomand, Joseph Bonica, Nima N. Naseri, Jean Paul G. Vonsattel, Hui Xu, Larry Park
Glucose metabolism is reduced in the brains of patients with Huntington disease (HD). The mechanisms underlying this deficit, its link to the pathology of the disease, and the vulnerability of the striatum in HD remain unknown. Abnormalities in some
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::31a7449d9d7b7c76c46bf53050656da0
https://europepmc.org/articles/PMC4435838/
https://europepmc.org/articles/PMC4435838/
Autor:
Arie Neymotin, Karen T. Liby, Elizabeth Wille, Renee Risingsong, Noel Y. Calingasan, M. Flint Beal, Michael B. Sporn, Nima N. Naseri, Maria Damiano, Mahmoud Kiaei, Susanne Petri
Oxidative damage, neuroinflammation, and mitochondrial dysfunction contribute to the pathogenesis of amyotrophic lateral sclerosis (ALS), and these pathologic processes are tightly regulated by the Nrf2/ARE (NF-E2-related factor 2/antioxidant respons
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::33ed3ee74ba394bb3082804e2046d02c
https://europepmc.org/articles/PMC3109235/
https://europepmc.org/articles/PMC3109235/
Lysosomal exocytosis releases pathogenic α-synuclein species from neurons in synucleinopathy models.
Autor:
Xie, Ying Xue, Naseri, Nima N., Fels, Jasmine, Kharel, Parinati, Na, Yoonmi, Lane, Diane, Burré, Jacqueline, Sharma, Manu
Publikováno v:
Nature Communications; 8/22/2022, Vol. 13 Issue 1, p1-16, 16p