Brain Mitochondrial ATP-insensitive large conductance Ca(+2)-activated K(+) channel properties are altered in a rat model of amyloid-β neurotoxicity.

Brain Mitochondrial ATP-insensitive large conductance Ca(+2)-activated K(+) channel properties are altered in a rat model of amyloid-β neurotoxicity. Exp Neurol. 2015 Mar 28; Authors: Jafari A, Noursadeghi E, Khodagholi F, Saghiri R, Sauve R, Aliaghaei A, Eliassi A Abstract Mitochondrial dysfunction is a hallmark of amyloid-beta (Aβ)-induced neuronal toxicity in Alzheimer's disease (AD). However, the underlying mechanism of how Aβ affects mitochondrial function remains uncertain. Because mitochondrial potassium channels have been involved in several mitochondrial functions including cytoprotection, apoptosis and calcium homeostasis, a study was undertaken to investigate whether the gating behavior of the mitochondrial ATP- and ChTx-insensetive-IbTx-sensitive Ca(2+)-activated potassium channel (mitoBKCa) is altered in a rat model of Aβ neurotoxicity. Aβ1-42 (4 μg/μl) was intracerebroventricularly injected in male Wistar rats (220-250). Brain Aβ accumulation was confirmed two weeks later on the basis of an immunohistochemistry staining assay, and physiological impacts measured in passive avoidance task cognitive performance experiments. Brain mitochondrial inner membranes were then extracted and membrane vesicles prepared for channel incorporation into bilayer lipid. Purity of the cell fraction was confirmed by Western blot using specific markers of mitochondria, plasma membrane, endoplasmic reticulum, and Golgi. Our res...
Source: Experimental Neurology - Category: Neurology Authors: Tags: Exp Neurol Source Type: research

Related Links:

In this study, researchers studied 438,952 participants in the UK Biobank, who had a total of 24,980 major coronary events - defined as the first occurrence of non-fatal heart attack, ischaemic stroke, or death due to coronary heart disease. They used an approach called Mendelian randomisation, which uses naturally occurring genetic differences to randomly divide the participants into groups, mimicking the effects of running a clinical trial. People with genes associated with lower blood pressure, lower LDL cholesterol, and a combination of both were put into different groups, and compared against those without thes...
Source: Fight Aging! - Category: Research Authors: Tags: Newsletters Source Type: blogs
Publication date: Available online 12 September 2019Source: Biochimica et Biophysica Acta (BBA) - BiomembranesAuthor(s): Angelique Camilleri, Stephanie Ghio, Mario Caruana, Daniel Weckbecker, Felix Schmidt, Frits Kamp, Andrei Leonov, Sergey Ryazanov, Christian Griesinger, Armin Giese, Ruben J. Cauchi, Neville VassalloAbstractMisfolding and aggregate formation by the tau protein has been closely related with neurotoxicity in a large group of human neurodegenerative disorders, which includes Alzheimer's disease. Here, we investigate the membrane-active properties of tau oligomers on mitochondrial membranes, using minimalist ...
Source: Biochimica et Biophysica Acta (BBA) Biomembranes - Category: Biochemistry Source Type: research
Snell dwarf mice in which growth hormone has been disabled live significantly longer than their peers. Suppression of growth hormone activity is one of the better studied interventions known to slow aging in mice, and, like calorie restriction, has led to a strong focus on stress response mechanisms in the aging research community. A majority of the means of slowing aging in short-lived laboratory species are characterized by increased cellular maintenance activities that are triggered into greater efforts by cellular stresses: heat, cold, lack of nutrients, an excess of toxic or reactive molecules, and so forth. De...
Source: Fight Aging! - Category: Research Authors: Tags: Daily News Source Type: blogs
We examined human lung tissue from COPD patients and normal control subjects, and found a substantial increase in p16-expressing alveolar cells in COPD patients. Using a transgenic mouse deficient for p16, we demonstrated that lungs of mice lacking p16 were structurally and functionally resistant to CS-induced emphysema due to activation of IGF1/Akt regenerative and protective signaling. Fat Tissue Surrounds Skeletal Muscle to Accelerate Atrophy in Aging and Obesity https://www.fightaging.org/archives/2019/09/fat-tissue-surrounds-skeletal-muscle-to-accelerate-atrophy-in-aging-and-obesity/ Researchers her...
Source: Fight Aging! - Category: Research Authors: Tags: Newsletters Source Type: blogs
Network-guided analysis of hippocampal proteome identifies novel proteins that colocalize with Aβ in a mice model of early-stage Alzheimer's disease. Neurobiol Dis. 2019 Sep 05;:104603 Authors: Caleb AA, Akiyama T, Kimura A, Kimura Y, Takahashi-Jitsuki A, Nakamura H, Makihara H, Masukawa D, Nakabayashi J, Hirano H, Nakamura F, Saito T, Saido T, Goshima Y Abstract Alzheimer's disease (AD) is an incurable neurodegenerative disease characterized by memory loss and neurotoxic amyloid beta (Aβ) plaques accumulation. Numerous pharmacological interventions targeting Aβ plaques accumulation hav...
Source: Neurobiology of Disease - Category: Neurology Authors: Tags: Neurobiol Dis Source Type: research
In this study were investigated the deregulated genes involved in mitophagy in the human periodontal ligament stem cells pretreated with moringin. The RNA-seq study reveals the downregulation of PINK1, with a fold change (FC) of −0.56, such as the genes involved in the phagophore formation (MAP1LC3B FC: −0.73, GABARAP FC: −0.52, GABARAPL1 FC: −0.70, GABARAPL2 FC: −0.39). The moringin pretreatment downregulates the pro−apoptotic gene BAX (−0.66) and upregulates the anti-apoptotic genes BCL2L12 (FC: 1.35) and MCL1 (FC: 0.36). The downregulation of the most...
Source: Molecules - Category: Chemistry Authors: Tags: Article Source Type: research
Progressive arterial stiffness with age causes hypertension, a state of chronically raised blood pressure, which in turn damages sensitive tissues in the brain and other organs. Over time that means a loss of function and cognitive decline. Researchers here suggest that even without the increase in blood pressure, stiffness in larger blood vessels will redistribute pressure in a way that will harm cells near to smaller capillary vessels. What causes arterial stiffening? A combination of damage and dysfunction such as, for example: persistent cross-links degrade elasticity in the extracellular matrix of blood vessel walls; ...
Source: Fight Aging! - Category: Research Authors: Tags: Daily News Source Type: blogs
In conclusion, in the absence of obesity, visceral adipose tissue possesses a pronounced anti-inflammatory phenotype during aging which is further enhanced by exercise. Methods of Inducing Cellular Damage are Rarely Relevant to Aging, and the Details Matter https://www.fightaging.org/archives/2019/08/methods-of-inducing-cellular-damage-are-rarely-relevant-to-aging-and-the-details-matter/ One of the major challenges in aging research is determining whether or not models of cellular or organismal damage and its consequences are in any way relevant to the natural processes of aging. One can hit a brick with...
Source: Fight Aging! - Category: Research Authors: Tags: Newsletters Source Type: blogs
Journal of Agricultural and Food ChemistryDOI: 10.1021/acs.jafc.9b03793
Source: Journal of Agricultural and Food Chemistry - Category: Food Science Authors: Source Type: research
Alzheimer's disease is the most prevalent neurodegenerative disorder leading to progressive cognitive decline. Despite decades of research, understanding AD progression at the molecular level, especially at its early stages, remains elusive. Here, we identified several presymptomatic AD markers by investigating brain proteome changes over the course of neurodegeneration in a transgenic mouse model of AD (3 ×Tg-AD). We show that one of these markers, heme-binding protein 1 (Hebp1), is elevated in the brains of both 3×Tg-AD mice and patients affected by rapidly-progressing forms of AD. Hebp1, predominantly expres...
Source: eLife - Category: Biomedical Science Tags: Neuroscience Source Type: research
More News: Alzheimer's | Brain | Calcium | Mitochondria | Mitochondrial Disease | Neurology | Study | Toxicology