Results 41 to 50 of about 50,997 (182)
Engineered GM1 Intersects Between Mitochondrial and Synaptic Pathways to Ameliorate ALS Pathology
Amyotrophic Lateral Sclerosis (ALS) is a fatal neurodegenerative disease driven by genetic and molecular disruptions affecting energy balance, protein homeostasis, and stress responses in nerve cells. Studies using human and rodent models identified convergent defects in mitochondria and synaptic function.
Federica Pilotto +11 more
wiley +1 more source
Loss of α-Synuclein Does Not Affect Mitochondrial Bioenergetics in Rodent Neurons. [PDF]
Increased α-synuclein (αsyn) and mitochondrial dysfunction play central roles in the pathogenesis of Parkinson's disease (PD), and lowering αsyn is under intensive investigation as a therapeutic strategy for PD. Increased αsyn levels disrupt mitochondria
Bendor, Jacob T +9 more
core +1 more source
A Natural Sweetener‐inducible Genetic Switch Controls Therapeutic Protein Expression in Mammals
This study develops a natural sweetener, the psicose‐inducible transgene expression (PURE) system based on an Agrobacterium tumefaciens–derived transcriptional repressor PsiR. The PURE system is highly specific to psicose, being insensitive to other sugars and structurally similar molecules.
Longliang Qiao +16 more
wiley +1 more source
MGST1, a GSH transferase/peroxidase essential for development and hematopoietic stem cell differentiation. [PDF]
We show for the first time that, in contrast to other glutathione transferases and peroxidases, deletion of microsomal glutathione transferase 1 (MGST1) in mice is embryonic lethal.
Abe, Hiroshi +10 more
core +3 more sources
Animal models remain indispensable in the study of pathological scars, each offering unique advantages and constraints. Their integration with in vitro and ex vivo systems is key to developing personalized, clinically translatable antifibrotic therapies. Abstract Pathological scarring, manifested in the form of hypertrophic scars (HTS) and keloid scars
Diana‐Larisa Ancuța +3 more
wiley +1 more source
Objective Mutations in TARDBP (encoding TDP‐43) are associated with the neurodegenerative disease amyotrophic lateral sclerosis (ALS) and include familial missense mutations where there are a lack of models and mechanisms examining how they are pathogenic.
Ziyaan A. Harji +10 more
wiley +1 more source
Reply to drs Bhatt and Hofmann [PDF]
Coment on : The maximum effective needle-to-nerve distance for ultrasound-guided interscalene block: an exploratory study. [Reg Anesth Pain Med. 2014]]]> interscalene block; patient eng oai:serval.unil.ch:BIB_7C5BB1A51EF1 2022-05 ...
Albrecht, Eric +3 more
core +1 more source
Objective De novo mutations in the syntaxin‐binding protein 1 (STXBP1), encoded by STXBP1, are among the most prevalent causes of variable neurodevelopmental disorders, including epileptic encephalopathy, developmental delay, and movement disorders.
Tao Yang +7 more
wiley +1 more source
Abstract The vertebrate skull is composed of bones derived from neural crest cells and mesoderm. The evolutionary capacity of the skull has been linked, in part, to the emergence of neural crest cells; however, this increased capacity for evolutionary change requires that variation within neural crest‐ and mesoderm‐derived bones remains partly ...
Alyssa C. Moore +5 more
wiley +1 more source
Imbalance of p75(NTR)/TrkB protein expression in Huntington's disease: Implication for neuroprotective therapies [PDF]
Neuroprotective therapies based on brain-derived neurotrophic factor (BDNF) administration have been proposed for Huntington's disease (HD) treatment. However, our group has recently reported reduced levels of TrkB in HD mouse models and HD human brain ...
Alberch, J. +5 more
core +1 more source

