The study, conducted by Hui-Chen Lu of the Department of Psy | Figure 1
The Study of NMNAT2 Production
The study, conducted by Hui-Chen Lu of the Department of Psychological and Brain Sciences at Indiana University and colleagues has shown that these compounds can increase the production of an enzyme known as NMNAT2, which may block processes associated with dementia.
In a previous study, the researcher had already demonstrated that the enzyme NMTAT2 offered protection to the brain against a type of stress and that it binds to Tau proteins, avoiding its incorrect folding.
For this study, the investigator and team sought to identify which compounds can increase the production of NMNAT2, thus increasing its protective effects.
One of the major compounds discovered to increase the production of NMNAT2 is caffeine, so the researchers then administered caffeine to mice that had been genetically engineered to produce low levels of NMNAT2. It was observed that the mice started to produce levels of that enzyme comparable to those of normal mice.
In the previous study, Hui-Chen Lu and team had found that mice that had been genetically modified to produce the incorrect folding of Tau proteins evidenced a low production of NMNAT2.
These findings may help in the development of new drugs for the prevention of Alzheimer's disease and other neurodegenerative diseases involving incorrect protein folding.
Source: Scientific Reports - Nature.
Detecting Alzheimer's Disease
Researchers at the Federal University of São Carlos (UFSCar) are developing a simple, quick and inexpensive method to detect Alzheimer's disease - something unheard of in the world.
For Professor Ronaldo Censo Faria, it is very difficult to differentiate Alzheimer's from other types of dementia. Usually, older people tend to have more dementias, 60% of which are related to Alzheimer's.
The new test is based on ADAM10 protein, present in blood, and shown to be altered in patients with Alzheimer's and mild neurocognitive disorder, considered a kind of pre-Alzheimer's.
The test is done by detecting the presence of this biomarker. The material used has a cost around $3, making it feasible to identify different stages of the disease and even a predisposition to Alzheimer's, according to the team.
A small amount of blood is treated with magnetic particles that are captured by a magnet. The concentration is determined with a disposable sensor device. The level of the biomarker tends to increase depending on the degree of disease.
Another advantage of the new examination is that current methods only detect the disease in more advanced stages. If diagnosed early, Alzheimer's treatment may be able to slow the progression of the disease, although there are still no fully effective therapies.
Source: Federal University of São Carlos.
Cheerin and Bone Loss
Results of experiments performed with mice suggest that inhibiting the action of the protein known as cheerin may present as an efficient strategy to prevent bone loss linked to inflammatory diseases. Burner is a molecule produced mainly by adipocytes, but is also expressed in several organs. There is evidence that this protein is increased in the bloodstream of people obese or suffering from type 2 diabetes, dyslipidemia, osteoporosis, rheumatoid arthritis, psoriasis, and Crohn's disease. Although the existence of a correlation between chronic inflammation, bone loss, and increase of burner was already evident, it was not yet established whether the molecule was only a marker or actively participated in the process that resulted in a decrease in bone mass.
According to Fukada, the molecule tested as a burner receptor antagonist is still in experimental use. Now we need to study the effect of quemerin on human osteoclasts to find out if we achieve the same effect.
Source: Journal of Bone and Mineral Research.
PPAR Delta Activation in Mice
The study, conducted by the Salk Institute for Biological Studies, USA, found that the activation of the gene known as PPAR delta (PPARD) in sedentary mice has reproduced the beneficial effects of aerobic exercise, which include fat burning and increased endurance.
However, the compound, which was administered to mice over a period of four weeks, while simulating maintenance of weight and insulin response, found in mice with the PPARD gene permanently activated, did not increase endurance.
For this study, the team decided to analyze whether higher doses of GW over a longer period could promote aerobic endurance and physical fitness.
The mice were tested on the treadmill, their aerobic endurance being compared to that of a control rodent group. It was observed that mice that had received GW had been able to exercise about 70% longer than those in the control group, that is, 270 minutes versus 160 minutes.
The team was surprised to find that genes suppressed in response to GW included those associated with the breakdown of carbohydrates used for energy, which they think indicates that the PPARD pathway causes sugar to stop being a source of energy for muscles during exercise, possibly to safeguard the brain.
Source: Cell Metabolism.