Results 41 to 50 of about 19,005 (175)
Abstract figure legend Suboptimal maternal nutrition alters placental and developing blood–brain barrier (BBB) protective function and is associated with increased fetal brain vulnerability. In the placenta, nutritional adversity may reduce the exchange surface area and promote meta‐inflammation, compromising barrier efficiency in a model‐ and context ...
Kristin L. Connor +4 more
wiley +1 more source
ABSTRACT Aim To test the hypothesis that Alzheimer‐like metabolic neurodegeneration rat model leads to an autonomic dysfunction, memory impairment, and hippocampal amyloid pathology and that long‐term chemogenetic stimulation of the dorsal motor nucleus of the vagus reverses these alterations. Methods Male and female transgenic Long Evans rats received
Beatriz Pacheco Sousa +2 more
wiley +1 more source
Altered expression of Alzheimer's disease-related proteins in male hypogonadal mice [PDF]
Age-related depletion of estrogens and androgens is associated with an increase in Alzheimer's disease (AD) brain pathology and diminished cognitive function. Here we investigated AD-associated molecular and cellular changes in brains of aged hypogonadal
Drummond, E.S. +3 more
core +2 more sources
In this work, we identified two novel pleiotropic sinapic acid derivatives with excellent anti‐acetylcholinesterase, antioxidant, and anti‐inflammatory properties. Alzheimer's disease, one of the most widespread neurodegenerative disorders, is known for its multifactorial nature that makes it challenging to treat.
Konstantina Sdougkou +2 more
wiley +1 more source
Double labelling immunohistochemical characterization of autonomic sympathetic neurons innervating the sow retractor clitoridis muscle [PDF]
Retrograde neuronal tracing and immunohistochemical methods were used to define the neurochemical content of sympathetic neurons projecting to the sow retractor clitoridis muscle (RCM). Differently from the other smooth muscles of genital organs, the RCM
Acone, Franca +6 more
core
A lifespan staging model of basal forebrain cholinergic vulnerability
Abstract The cholinergic neurons of the basal forebrain are among the most vulnerable cell types to age‐ and Alzheimer's disease‐related dysfunction and neurodegeneration. However, the biological bases of basal forebrain cholinergic vulnerability (the why) and the temporal sequence (the how) have yet to be fully resolved.
Hayley R. C. Shanks +3 more
wiley +1 more source
Human tenocytes are stimulated to proliferate by acetylcholine through an EGFR signalling pathway [PDF]
Studies of human patellar and Achilles tendons have shown that primary tendon fibroblasts (tenocytes) not only have the capacity to produce acetylcholine (ACh) but also express muscarinic ACh receptors (mAChRs) through which ACh can exert its effects. In
Alexander Scott +4 more
core +1 more source
Stem cell therapy for Alzheimer's disease: hype or hope? [PDF]
Alzheimers disease (AD) is the most common neurodegenerative disease affecting millions of people in the world. Cognitive impairments such as progressive memory loss are devastating manifestations from this disease.
Liu, AKL
core +1 more source
Chemical Metabolomics: Chemical Biology Tools for Advanced Metabolism Investigations
The human metabolism has been investigated for several millennia. The metabolome is known for a high complexity due to a large number of different metabolites that are present at different concentrations. Metabolomics has been developed as a field to investigate the entire human metabolome and to elucidate disease development mechanisms.
Alejandro Torregrosa‐Chinillach +4 more
wiley +1 more source
Regulated peristalsis into the acidic region of the _Drosophila_ larval midgut is controlled by a novel component of the Autonomic Nervous System [PDF]
The underlying cellular and molecular mechanisms that regulate and coordinate critical physiological processes such as peristalsis are complex, often cryptic, and involve the integration of multiple tissues and organ systems within the organism.
Brooke Ann Johnson +4 more
core +1 more source

