Are abnormal intestinal microorganisms a risk factor for developing cognitive impairment? Researchers at Rush University Medical Center are trying to answer that question with a new study that will explore how the intestinal microbiota – the bacteria in the intestine –influence the progression of cognitive decline and the development of Alzheimer’s disease.
Health care providers and researchers increasing are recognizing that the intestinal microbiota – also known as the microbiome – affects health. The human intestine contains tens of trillions of microorganisms, and humans have developed a symbiotic relationship with these bacteria in.
Food consumption by humans provides food/energy to this intestinal bacteria, which in turn influence health by producing numerous biologically relevant substances, including vitamins, and strongly influence the immune system. Studies show that the intestinal microbiota also influences the brain.
For example, changes in the intestinal microbiota can influence anxiety- and depression-like symptoms in rodents and can promote brain pathology in a mouse model of Parkinson’s disease.
Changing our behavior based on unexpected cues from our environment is an essential part of survival. The ability to drop what you’re doing when circumstances demand it could mean the difference between avoiding a speeding vehicle or getting hit by it. A new study at the Okinawa Institute of Science and Technology Graduate University (OIST) has delved into a brain mechanism that may regulate such adaptation.
In the study, which was published in eLife, researchers led by Dr. Stefano Zucca at the OIST Neurobiology Research Unit investigated nerve cells in the striatum, a brain region involved in movement and motivation. Here, nerve cells called cholinergic interneurons (CINs) are in a near-constant state of activity, releasing a chemical called acetylcholine every time they fire. But if the brain gets an unexpected stimulus from outside the body – for example, a startling sound – the CINs will briefly stop firing.
Researchers have shown how cholesterol – a molecule normally linked with cardiovascular diseases – may also play an important role in the onset and progression of Alzheimer’s disease.
The international team, led by the University of Cambridge, have found that in the brain, cholesterol acts as a catalyst which triggers the formation of the toxic clusters of the amyloid-beta protein, which is a central player in the development of Alzheimer’s disease.
The results, published in the journal Nature Chemistry, represent another step towards a possible treatment for Alzheimer’s disease, which affects millions worldwide. The study’s identification of a new pathway in the brain where amyloid-beta sticks together, or aggregates, could represent a new target for potential therapeutics.
It is unclear if the results have any implications for dietary cholesterol, as cholesterol does not cross the blood-brain barrier. Other studies have also found an association between cholesterol and the condition, since some genes which process cholesterol in the brain have been associated with Alzheimer’s disease, but the mechanism behind this link is not known.
The Cambridge researchers found that cholesterol, which is one of the main components of cell walls in neurons, can trigger amyloid-beta molecules to aggregate. The aggregation of amyloid-beta eventually leads to the formation of amyloid plaques, in a toxic chain reaction that leads to the death of brain cells.
Alzheimer’s disease, a severely debilitating and ultimately fatal brain disorder, affects millions worldwide. To date, clinical efforts to find a cure or adequate treatment have met with dispiriting failure.
The disease is now on an ominous course of expansion, due in part to an aging population, and is poised to become a global health emergency. The enigmatic ailment–first described over 100 years ago–remains the only leading killer without effective treatment, prevention or cure.
In a new study, researchers at the ASU-Banner Neurodegenerative Disease Research Center examine the effects of the disease on the functioning of mitochondria–structures performing a variety of essential tasks, including supplying cells with energy.
The new research reveals that a highly toxic form of beta amyloid protein– known as oligomeric a-beta (OAβ)–disrupts the normal functioning of mitochondria. The result is a fateful cascade of events that appears early in the development of Alzheimer’s disease–decades before the onset of clinical symptoms.
The most promising finding in the new study is that human neuronal cells can be protected from OAβ-induced deterioration of their mitochondria when they are pre-treated with a custom-designed compound, suggesting an exciting avenue for future drug targeting.
“Mitochondria are the major source of energy in brain cells and deficiencies in energy metabolism have been shown to be one of the earliest events in Alzheimer’s disease pathobiology. This study reinforces the toxicity of oligomeric amyloid beta on neuronal mitochondria and stresses the importance for protective compounds to protect the mitochondria from oligomeric amyloid beta toxicity,” said Diego Mastroeni, a lead author of the new study.