Study: Impaired fat breakdown in the brain leads to measurable dumbing down

Study: Impaired fat breakdown in the brain leads to measurable dumbing down

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Impaired fat loss in the brain makes mice dumb
Impaired fat loss in the brain has an extremely adverse effect on learning and memory, according to the results of a recent study led by scientists from the University of Bonn. The study results also take a new look at the development of dementia, reports University.

According to the researchers, the impaired breakdown of certain fat molecules in the brain significantly affects learning and memory performance - at least in mice. In model experiments, the animals showed significantly poorer learning and memory performance when the fat loss was impaired. In addition, the amount of Alzheimer's-specific proteins in her brain has risen sharply, the scientists report. The researchers published their results in the specialist magazine "Autophagy".

Brain is real
In the experiments, the scientists prevented the breakdown of a certain fat molecule in the mouse brain. Because according to the researchers, the proverbial "brain fat" actually exists. So apart from water, the brain consists mainly of lipids, in simple terms: fat. These lipids serve, for example, "as an insulating layer around the nerve fibers and thus prevent short circuits," the experts explain. They are also a key component of the thin membrane membranes that surround the brain cells.

Mice learn and remember less well
One of the most common lipids in our brain is the so-called sphingolipid, whose breakdown product S1P may play a central role in the development of Alzheimer's and other dementias, the researchers explain. For their experiments, they bred mice "that can no longer break down S1P in large parts of their brains," said Dr. Gerhild van Echten-Deckert from the LIMES Institute at the University of Bonn. As a result, "the animals learned much worse and could not remember as well," the university reports.

Mechanism of autophagy disrupted
According to the researchers, the S1P is normally broken down into various parts, with one of the breakdown products being urgently needed for another metabolic pathway - so-called autophagy. This mechanism enables cells to digest and recycle their own components. In this way, the cells can, for example, remove defective proteins or cell organelles that no longer fulfill their task.

Breakdown product of S1P needed for autophagy
According to the scientists, intracellular garbage disposal in autophagy works in two steps. First, the "waste" is packed in tiny "garbage bags", which then fuse with other "bags" that contain highly reactive enzymes. These enzymes then “shred” the contents of the garbage bags and dispose of them, the researchers explain. A waste product from S1P is involved in the packaging of the waste in the intracellular garbage bags, and “without the breakdown of S1P, less closed garbage bags form; autophagy will then no longer function properly, ”says study author Daniel Mitroi in the press release from the University of Bonn.

Accumulation of harmful substances in the brain
When S1P breakdown is switched off, harmful substances have accumulated in the mice's brain, such as “the protein APP, which plays a key role in the development of Alzheimer's disease,” reports the first author of the study.

Unknown mechanism of origin for dementia discovered?
According to the researchers, the current study results focus on a hitherto completely unnoticed development mechanism for dementia. For the first time, scientists from the University of Bonn, the University Hospital Jena, the German Center for Neurodegenerative Diseases (DZNE) and from San Francisco and Madrid were able to show the far-reaching consequences of the impaired S1P breakdown. "In the long term, our work may contribute to the fact that these brain disorders can be successfully treated at some point," said Dr. van Echten-Deckert. (fp)

Author and source information

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