You find that our brains contain lithium – and its loss may help to push Alzheimer’s disease

Alzheimer’s disease is one of the most harsh conditions that a person can develop. Even with recent developments, there is much but much to do as soon as its symptoms appear. External research this week may highlight a decisive and previously lost factor that leads the disease, which may even lead to new treatments.

Scientists at Harvard University Medical Faculty led the study, Published Wednesday in nature. By studying human brain and mice, they found evidence that our brains naturally contain a lithium element – and that its deficiency can help explain the damage caused by Alzheimer’s disease. An external expert, an external expert, told Gizmodo.

The study researchers “conducted detailed and well designed studies to investigate the extent of lower lithium levels (Alzheimer’s disease) associated with the levels of diagnosis, protein, cellular and genes.” Zhang is also the director of the Alzheimer’s disease center in California at the University of California, Los Angeles.

The brains of people with Alzheimer’s disease are different from others. In particular, it contains high levels of the wrong amyloid beta and theo, two protein that have important functions usually. But these are not the only changes seen in Alzheimer’s disease. During the investigation of these other changes discovered by Harvard University researchers.

With the help of current projects that collected post -death tissue samples, they compared the levels of about 30 minerals in the brains of people who died along different stages of cognitive health. It was the only main difference that he found with lithium. People with healthy brains had relatively high levels of lithium, while those with Alzheimer’s disease had much lower levels. More importantly, this lithium loss was evident even in people who had mild memory problems before death.

The researchers also studied healthy mice and genetically modified mice that develop a copy of Alzheimer’s disease. When they exhausted lithium from these mice, it seemed that it accelerated the accumulation of unhealthy amyloid and more in the brain, along with low memory. They also found evidence that this loss is caused by the amyloid beta -associated beta plaques in the brain and that this lithium loss negatively affects all types of the main cells in the brain.

Although there are some limited research suggestion Among the potential relationship between lithium and Alzheimer’s, the authors say they are the first to show that our brains are normal. Moreover, their results hint that lithium is necessary for good brain health and that its absence is the key to the development of Alzheimer’s disease.

“This is the first study that indicates that lithium deficiency may contribute to Alzheimer’s disease. The reason for this was not suggested is that he did not think that lithium is a natural substance in the brain with biological effect, just a drug with drug effects on high doses, Professor Bruce Yannner, Professor in genetics in the science of school equipped in Harvard. “As such, this study is the first to explore the consequences of lithium deficiency in the brain.”

The effects of this study, although they are still early, can definitely be exciting. Yankner and his team also enabled the lithium compound that was not easily bound by the amyloid beta. When they gave mice (ancient healthy mice and mice with Alzheimer’s disease) this compound, it appears to prevent harmful brain changes and memory loss usually with the condition of nervous degeneration. Even the best on the amyloid Treatments In contrast, for Alzheimer’s available today, in contrast to that, its progress is delayed modestly.

Other forms of lithium are used in medicine to treat some mental health disorders, especially depression. But these versions require high doses to work as intended and come with many side effects as a result. However, the team complex asks a much lower dose to be effective in mice, and no sign of toxicity was noticed at all.

“It is necessary to conduct more clinical studies in humans to assess whether the correct type and dosage of lithium can prevent or slow Alzheimer’s disease,” Zhang noted.

Yankner and his team are now forward with the research needed to show their complex (or something similar) that can be safely tested in human clinical experiences. But even before that, the team’s discovery can be paid in other ways. Alzheimer’s risks may be possible by measuring lithium levels for people, for example. There are still many remaining puzzles for lithium jak and its role in brain health.

“As a neuroscientist, I am excited to explore the physiology of lithium in the brain,” said Yankanner. “I think we have scratched the surface of what will be some very interesting biology.”