Impairment of brain function in a mouse model of Alzheimer's disease during the pre-depositing phase: The role of α7 nicotinic acetylcholine receptors.

Alzheimer's disease (AD) is an age-dependent incurable neurodegenerative disorder accompanied by neuroinflammation, amyloid accumulation, and memory impairment. It begins decades before the first clinical symptoms appear, and identifying early biomarkers is key for developing disease-modifying therapies. We show now in a mouse model of AD that before any amyloid deposition the brains of 1.

Agonists or positive allosteric modulators of α7 nicotinic acetylcholine receptor prevent interaction of SARS-Cov-2 receptor-binding domain with astrocytoma cells.

SARS-Cov-2, the virus causing COVID-19, penetrates host target cells via the receptor of angiotensin-converting enzyme 2 (ACE2). Disrupting the virus interaction with ACE2 affords a plausible mechanism for prevention of cell penetration and inhibiting dissemination of the virus. Our studies demonstrate that ACE2 interaction with the receptor binding domain of SARS-Cov-2 spike protein (RBD) can be impaired by modulating the α7 nicotinic acetylcholine receptor (α7 nAChR) contiguous with ACE2.

Hydroxyurea interaction with α7 nicotinic acetylcholine receptor can underlie its therapeutic efficacy upon COVID-19.

In this paper the authors provide evidence that hydroxyurea (hydroxycarbamide) interacts with α7 nicotinic acetylcholine receptor, exerts anti-inflammatory and pro-survival effect, prevents α7 nicotinic receptor interaction with angiotensin-converting enzyme-2 and stimulates IgM to IgG class switch upon immunization with SARS spike protein fragment 674-685. Hydroxyurea shifts immunoglobulin glycosylation profile to anti-inflammatory phenotype and prevents the appearance of anti-idiotypic α7(179-190)-specific antibodies, as well as memory impairment. According to these results, interaction with α7 nicotinic acetylcholine receptor may underlie positive therapeutic effects of hydroxyurea upon SARS-Cov-2 infection by interfering with virus penetration into the cell and providing anti-inflammatory and immunomodulatory effects.

α7 Nicotinic acetylcholine receptors regulate translocation of HIF-1α to the cell nucleus and mitochondria upon hypoxia.

Nicotinic acetylcholine receptors (nAChRs), initially characterized as ligand-gated ion channels mediating fast synaptic transmission, are now found in many non-excitable cells and mitochondria where they function in ion-independent manner and regulate vital cellular processes like apoptosis, proliferation, cytokine secretion. Here we show that the nAChRs of α7 subtype are present in the nuclei of liver cells and astrocytoma U373 cell line. As shown by lectin ELISA, the nuclear α7 nAChRs are mature glycoproteins that follow the standard rout of post-translational modifications in Golgi; however, their glycosylation profile is non-identical to that of mitochondrial nAChRs.

An Leaf Diet Influences Myogenin Gene Expression, Performance, and Carcass Characteristics in Lambs.

Myogenin is a protein in the myogenic regulatory factor family that plays an important role in determining carcass and meat traits and is vital for the growth and development of livestock muscles. The objective of this study was to determine the impact of Origanum majorana leaf (MOL) on the myogenin gene expression of lambs. Twenty-four male Kermani lambs were used in a completely randomized design using two experimental groups (0% Origanum majorana L.