Results 111 to 120 of about 129,516 (303)

CARD9 Conveys Pancreatic Islet Sympathetic Nervous β2 Signals to Reshape Macrophage Creatine Metabolism in Type 1 Diabetes

open access: yesAdvanced Science, Volume 13, Issue 3, 14 January 2026.
This study identifies CARD9 as a key mediator linking sympathetic β2‐adrenergic receptor signaling to macrophage creatine metabolism, inflammatory polarization, and neuronal integrity. Loss of β2‐AR‐PKA‐CREB1‐CARD9 signaling in macrophages reduces creatine uptake, promotes pro‐inflammatory macrophage activation, and drives sympathetic axon ferroptosis.
Huimin Yuan   +12 more
wiley   +1 more source

Simultaneous release of glutamate and acetylcholine from single magnocellular "cholinergic" basal forebrain neurons [PDF]

open access: yes, 2006
Basal forebrain (BF) neurons provide the principal cholinergic drive to the hippocampus and cortex. Their degeneration is associated with the cognitive defects of Alzheimer's disease. Immunohistochemical studies suggest that some of these neurons contain
Abogadie, FC, Allen, TGJ, Brown, DA
core   +1 more source

Metabolism‐Regulating Nanomedicines for Cancer Therapy

open access: yesAdvanced NanoBiomed Research, Volume 6, Issue 1, January 2026.
This review highlights metabolism‐regulating nanomedicines designed to target glycolytic, lipid, amino acid, and nucleotide pathways in tumors. By incorporating metabolism‐regulating agents into versatile nanocarriers such as liposomes, micelles, dendrimers, and engineered bacteria, these platforms achieve targeted delivery, controlled release ...
Xiao Wu, Shiyi Geng, Jian Yang
wiley   +1 more source

Cholinergic cells in the nucleus basalis of mice express the N-methyl-D-aspartate-receptor subunit NR2C and its replacement by the NR2B subunit enhances frontal and amygdaloid acetylcholine levels [PDF]

open access: yes, 2006
It is known that glutamatergic and cholinergic systems interact functionally at the level of the cholinergic basal forebrain. The N-methyl-D-aspartate receptor (NMDA-R) is a multiprotein complex composed of NR1, NR2 and/or NR3 subunits.
Broide R.S.   +11 more
core   +2 more sources

Engineering Liposomes for Neurodegenerative Diseases: Targeted Delivery and Regenerative Potential

open access: yesChemNanoMat, Volume 12, Issue 1, January 2026.
Liposomal nanocarriers offer therapeutic promise for neurodegenerative diseases by encapsulating diverse agents such as neurotrophic factors and mRNA while targeting the blood‐brain barrier. Designed to stimulate neuronal repair and restore function, these lipid vesicles advance strategies for optimized design and central nervous system delivery ...
Oybek Ashirov   +3 more
wiley   +1 more source

Glucagon-Like Peptide-1 Modulates Neurally-Evoked Mucosal Chloride Secretion in Guinea Pig Small Intestine In Vitro. [PDF]

open access: yes, 2011
Glucagon-like peptide-1 (GLP-1) acts at the G protein-coupled receptor, GLP-1R, to stimulate secretion of insulin and to inhibit secretion of glucagon and gastric acid. Involvement in mucosal secretory physiology has received negligible attention. We
BALDASSANO, Sara   +3 more
core   +1 more source

Lineage‐Biased Neural Stem Cell Grafting Promotes Neuronal Differentiation and Vascular Repair in the Chronic Phase of Stroke

open access: yesCNS Neuroscience &Therapeutics, Volume 32, Issue 1, January 2026.
Schematic diagram comparing two differentiation strategies to generate NSCs. The nEB‐NSCs exhibited a pronounced bias toward neuronal lineage differentiation. Transplantation of nEB‐NSCs into stroke mice (induced by tMCAO surgery) promoted motor recovery and vascular repair.
Tingting Zhang   +7 more
wiley   +1 more source

TTBK2‐Driven Ciliogenesis Is Required for Intrinsic Neuronal Regeneration After Spinal Cord Injury

open access: yesCNS Neuroscience &Therapeutics, Volume 32, Issue 1, January 2026.
TTBK2‐dependent ciliogenesis is required for intrinsic neuronal regeneration after spinal cord injury. Loss of TTBK2 disrupts primary cilium integrity, attenuates SHH signaling, and impairs axonal regrowth. Restoring SHH activity partially rescues neuronal structural deficits, highlighting the TTBK2/cilium–SHH as a therapeutic target.
Renfeng Zhang   +6 more
wiley   +1 more source

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