4-Phenylbutyric acid attenuates amyloid-β proteotoxicity through activation of HSF-1 in an Alzheimer's disease model of the nematode Caenorhabditiselegans.

Alzheimer's disease (AD) is a neurodegenerative disorder and the most common form of dementia. The pathogenesis is a complex process, in which the proteotoxicity of amyloid-β (Aβ) was identified as a major factor. 4-Phenylbutyric acid (4-PBA) is an aromatic short-chain fatty acid that may attenuate Aβ proteotoxicity through its already shown properties as a chemical chaperone or by inhibition of histone deacetylases (HDACs).

Caprylic acid attenuates amyloid-β proteotoxicity by supplying energy via β-oxidation in an Alzheimer's disease model of the nematode .

Computer-based analysis of motility was used as a measure of amyloid-β (Aβ) proteotoxicity in the transgenic strain GMC101, expressing human Aβ in body wall muscle cells. Aβ-aggregation was quantified to relate the effects of caprylic acid (CA) to the amount of the proteotoxic protein. Gene knockdowns were induced through RNA-interference (RNAi).

RNA-interference in the nematode Caenorhabditis elegans is effective using paraformaldehyde-inactivated E. coli HT115 bacteria as a food source.

The nematode Caenorhabditis elegans is a widely used research model for the investigation of metabolism, aging and age-associated diseases. However, when investigating the impact of natural compounds or drugs on those topics, a major confounder is the metabolism of these test substances by live E. coli bacteria, the standard food source of C.

Extracorporeal life support in patients with acute myocardial infarction complicated by cardiogenic shock - Design and rationale of the ECLS-SHOCK trial.

Background: In acute myocardial infarction complicated by cardiogenic shock the use of mechanical circulatory support devices remains controversial and data from randomized clinical trials are very limited. Extracorporeal life support (ECLS) - venoarterial extracorporeal membrane oxygenation - provides the strongest hemodynamic support in addition to oxygenation. However, despite increasing use it has not yet been properly investigated in randomized trials.

Infertility induced by auxin in PX627 does not affect mitochondrial functions and aging parameters.

is widely used for aging studies. 5-Fluoro-2´-deoxyuridine (FUdR) is commonly used to control offspring. While larvae are stopped from further development, also mitochondrial DNA and function may be affected.

Amyloid-beta (Aβ)-induced paralysis in Caenorhabditis elegans is reduced through NHR-49/PPARalpha.

Alzheimer´s disease is a neurodegenerative disorder characterized by the misfolding and aggregation of amyloid β (Aβ). Agonists of peroxisomal proliferator-activated receptors (PPARs) are discussed as anti-amyloidogenic compounds, e.g.

Mitochondrial Oxidative Stress Impairs Energy Metabolism and Reduces Stress Resistance and Longevity of .

Introduction: Mitochondria supply cellular energy and are key regulators of intrinsic cell death and consequently affect longevity. The nematode is frequently used for lifespan assays. Using paraquat (PQ) as a generator of reactive oxygen species, we here describe its effects on the acceleration of aging and the associated dysfunctions at the level of mitochondria.

Amyloid-beta induced paralysis is reduced by cholecalciferol through inhibition of the steroid-signaling pathway in an Alzheimer model of .

Alzheimer's disease (AD) is a neurodegenerative disorder resulting from the accumulation of toxic β-amyloid (Aβ) aggregates in the human brain. Epidemiological studies have shown that elevated cholesterol plasma levels are associated with the development of AD and we have previously shown that cholesterol restriction reduces the Aβ-induced paralysis in an Alzheimer model of the nematode In the present study we investigated the effects of the cholesterol homolog cholecalciferol, i.e.