Results 91 to 100 of about 12,300 (184)

Macromolecule‐Loaded Hybrid Extracellular Vesicles via Ionic Lipid–Based Post‐Loading for Intracellular Delivery: Functional Evaluation for Neurodegenerative Therapy

Journal of Extracellular Biology, Volume 5, Issue 3, March 2026.
ABSTRACT Extracellular vesicles (EVs) are natural carriers that show promise as drug delivery systems (DDS). We developed a non‐invasive post‐loading method to encapsulate macromolecules in EVs using our proprietary ionic lipid base (ILB), which enables electrostatically driver hybridisation without disrupting EV structure.
Lin Cui, Fumiyasu Ono, Tomoko Ichinose, Masahiro Goto, Kohei Ishihama   +4 more
wiley   +1 more source

Reduced Dietary Protein Induces Changes in the Dental Proteome

Journal of Experimental Zoology Part B: Molecular and Developmental Evolution, Volume 346, Issue 2, Page 107-127, March 2026.
Low dietary protein (10%) from normal (20%) does change protein expression in tooth proteome and alter developmental pathways. Among the significant protein expressions changes are actin‐based myosins, tooth, and bone development proteins. Perplexingly tooth size is not altered, suggesting more nuanced phenotypic response to low dietary protein in ...
Robert W. Burroughs, Christopher J. Percival, Natasha S. Vitek   +2 more
wiley   +1 more source

Tyrosine Hydroxylase Deficiency Impairs TH Axonal Transport, Brain Function, and Neuronal Plasticity

Journal of Inherited Metabolic Disease, Volume 49, Issue 2, March 2026.
ABSTRACT Tyrosine hydroxylase deficiency (THD) is a rare genetic disorder caused by biallelic pathogenic variants in the Th gene, leading to a deficiency in the rate‐limiting enzyme for the synthesis of dopamine (DA) and other catecholamine neurotransmitters.
Tie‐Jun Sten Shi, Kunwar Jung‐KC, Gong‐Wei Lyu, Liang Han, Ming Ying, Beat Thöny, Aurora Martinez   +6 more
wiley   +1 more source

Re‐conceptualizing Parkinson's disease as a lifelong neurobiological trajectory: A framework for prevention

Neuroprotection, Volume 4, Issue 1, Page 14-29, March 2026.
Three‐panel graphical abstract showing the Lifelong Neurobiological Trajectory framework for Parkinson's disease: (1) Vulnerability pathway (top, red) showing how early adversity → epigenetic dysregulation, neuroinflammation, and mitochondrial dysfunction → ↑ PD risk; (2) Lifespan timeline (middle, purple) spanning prenatal/infancy → childhood ...
Ayodeji Johnson Ajibare, Abraham Olufemi Asuku, Olabode Oluwadare Akintoye   +2 more
wiley   +1 more source

α-Synuclein (SNCA) [PDF]

Science-Business eXchange, 2009
openaire   +3 more sources

Analysis of α-syn and parkin interaction in mediating neuronal death in Drosophila model of Parkinson's disease

Frontiers in Cellular Neuroscience
One of the hallmarks of Parkinson's Disease (PD) is aggregation of incorrectly folded α-synuclein (SNCA) protein resulting in selective death of dopaminergic neurons.
Sonia Narwal, Amit Singh, Meghana Tare
doaj   +1 more source

Neuronal-type-specific epigenome editing to decrease SNCA expression: Implications for precision medicine in synucleinopathies

Molecular Therapy: Nucleic Acids
Overexpression of SNCA has been implicated in the pathogenesis of synucleinopathies, particularly Parkinson’s disease (PD) and dementia with Lewy bodies (DLB).
Zhiguo Sun, Boris Kantor, Ornit Chiba-Falek   +2 more
doaj   +1 more source

SNCA Gene [PDF]

, 2020
openaire   +1 more source

SNCA wt Allele [PDF]

, 2020
openaire   +1 more source

PLK2 disrupts autophagic flux to promote SNCA/α-synuclein pathology

Autophagy
The aggregation and transmission of SNCA/α-synuclein (synuclein, alpha) is a hallmark pathology of Parkinson disease (PD). PLK2 (polo like kinase 2) is an evolutionarily conserved serine/threonine kinase that is more abundant in the brains of all family members, is highly expressed in PD, and is linked to SNCA deposition.
Chuang Zhang, Zhanpeng Huang, Xinyue Huang, Yanni Ma, Yifan Cao, Zhixiong Zhang, Rui Wang, Haigang Ren, Longtai Zheng, Chun-Feng Liu, Guanghui Wang   +10 more
openaire   +2 more sources