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Scientists at Osaka Metropolitan University By studying the effects of the antibiotic rifampicin on transgenic mice in amyotrophic lateral sclerosis (ALS) and another brain disease frontotemporal An important step forward in the prevention of leaf dementia (FTD). Their paper was published in the journal Biomedicines.
Research published in Biomedicines on May 6, 2022 (latest impact factor: 6.0)
“The main cause of frontotemporal dementia and amyotrophic lateral sclerosis is hexanucleotide repeat expansion (HRE) in the noncoding region of C9orf72 gene,” said lead researcher Professor Takami Tomiyama. This mutation leads to neurodegeneration through loss-of-function or toxic-function mutation. “Loss-of-function mutations manifest as the formation of a nucleic acid structure called a G-quadruplex that blocks transcription of C9orf72.” Toxic gain-of-function mutations manifest as RNA foci, toxic RNA aggregates, and dipeptide repeat proteins (DPRs) ) formation,” explains Prof. Tomiyama. G-quadruplex and DPR together further accelerate the aggregation of RNA-binding proteins such as TDP-43, leading to neurodegeneration.
Rifampicin is an antibiotic that slows down the production of bacterial RNA and is usually given in combination with other antibiotics. Examining the effect of rifampicin on the formation of RNA foci, DPR and TDP-43 inclusions, the research team determined its potential to prevent FTD and ALS. They used human 500 hexanucleotide repeat expansions Rifampicin was administered nasally to the mice using the C9orf72 gene. The team then assessed their cognitive function by observing their ability to escape the maze before examining the mice’s brain tissue.
p>Rifampicin treatment can significantly improve cognitive function and memory function in transgenic c9orf72 mice
The results showed that, Nasal rifampicin treatment significantly improves cognitive function and memory in mice. It greatly inhibits the formation of cytoplasmic inclusions composed of protein aggregates in brain tissue. Rifampicin also attenuated the formation of RNA foci containing G-quadruplexes, although the mechanism of action is unclear. In addition, synaptic loss, neuronal loss and microglial activation were also attenuated by rifampicin treatment.
This study is the latest in a series of articles by researchers about the effects of rifampicin in the prevention of neurological disorders. Professor Tomiyama concluded: “We have previously demonstrated in model mice that nasal rifampicin is effective against dementias such as Alzheimer’s disease, tau-related frontotemporal dementia and Lewy Dementia. This time, however, it was found to be effective in the onset and progression of FTD and ALS caused by the C9orf72 gene. Rifampicin may be a broadly effective drug for preventing neurodegenerative diseases /strong>.”
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References
Source: Osaka Metropolitan University
Stopping C9orf72-linked dementia in mutant mice with antibiotic rifampicin
Reference:
Yukari Hatanaka et al, C9orf72 Hexanucleotide Repeat Expansion-Related Neuropathology Is Attenuated by Nasal Rifampicin in Mice, Biomedicines ( 2022). DOI: 10.3390/biomedicines10051080
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