Results 211 to 220 of about 78,455 (315)

Harnessing controlled human infection models to accelerate vaccine development for neglected tropical diseases: Lessons from leishmaniasis

open access: yesEuropean Journal of Clinical Investigation, Volume 56, Issue 1, January 2026.
Controlled Human Infection Models (CHIMs) offer a powerful approach to accelerate vaccine development for neglected tropical diseases (NTDs). This review highlights scientific and translational advances enabled by CHIMs, with a focus on a novel Leishmania major model.
Vivak Parkash
wiley   +1 more source

Reactive astrocytes in prion diseases: Friend or foe? [PDF]

open access: yesPLoS Pathog
Makarava N, Kushwaha R, Baskakov IV.
europepmc   +1 more source

Proteostasis unbalance in prion diseases: Mechanisms of neurodegeneration and therapeutic targets. [PDF]

open access: yesFront Neurosci, 2022
Thellung S   +5 more
europepmc   +1 more source

Hydrophobic residues in the α‐synuclein NAC domain drive seed‐competent fibril formation and are targeted by peptide inhibitors

open access: yesThe FEBS Journal, Volume 293, Issue 1, Page 134-155, January 2026.
The hydrophobic 68GAVV71 stretch in the NAC domain of α‐synuclein is essential for nucleation, while residues 79–95 are required for fibril stability and seeding. Truncation or inhibition of 68GAVV71 prevents fibril formation, and truncation of 79–95 abolishes seeding competency, highlighting their distinct roles in α‐synuclein aggregation and ...
Viswanath Das   +13 more
wiley   +1 more source

Post-translational modifications in prion diseases. [PDF]

open access: yesFront Mol Neurosci
Bizingre C   +5 more
europepmc   +1 more source

'Prion' Diseases

open access: yesJournal of the Royal College of Physicians of London, 1994
openaire   +2 more sources

TDP‐43 proteinopathies and neurodegeneration: insights from Caenorhabditis elegans models

open access: yesThe FEBS Journal, Volume 293, Issue 2, Page 348-384, January 2026.
The manuscript explores structural and functional features of TDP‐43 and its worm homologue, TDP‐1, highlighting conserved and divergent structural and functional features. Using genetically engineered C. elegans models, key pathological features of TDP‐43 proteinopathies—including aggregation, neurodegeneration, and motor deficits—are recapitulated ...
Ghulam Jeelani Pir   +7 more
wiley   +1 more source

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