Sunday, December 18, 2016
Antibiotic Rocephin May Restore Brain Function In Alzheimer’s Disease, Study Suggests
Treatment with the antibiotic Rocephin (ceftriaxone) may restore brain function in areas affected by Alzheimer’s disease, according to new research.
The study, “Mapping Synaptic Glutamate Transporter Dysfunction In Vivo To Regions Surrounding Aβ Plaques By Iglusnfr Two-Photon Imaging,” was published in the journal Nature Communications.
The hallmark of Alzheimer’s disease is the production of beta-amyloid protein plaques, which accumulate in neurons, disrupting their activity and communication.
Researchers found that in brain areas where beta-amyloid protein plaques are present there also is an increased amount of glutamate (a molecule that neurons use to send signals each other to communicate) and increased activity of glial cells, which surround and support neurons. These alterations promote dysregulated neuronal activity and cause neuronal damage and loss in advanced stages of the disease.
Previous studies have shown that the antibiotic Rocephin was able to improve glutamate and prevent its accumulation, in neurons. Thus, researchers administered the antibiotic to mice with Alzheimer’s disease. Results showed that, indeed, Rocephin resolved the accumulation of glutamate and restored its levels to normal, subsequently improving neuronal communication in areas affected by the plaques.
“By imaging the glial cells and glutamate itself around the plaques, we were able to see that the cells were not able to ‘remove’ the glutamate accumulating in these brain areas. By using [Rocephin], we were able to [increase] glutamate transport,” Brian MacVicar, , the study’s senior author, said in a press release. “By restoring glutamate levels, we were able to mostly restore neuronal activity.”
The team believes that targeting the toxic accumulation of glutamate in neurons affected by beta-amyloid plaques may be a promising strategy to treat the early symptoms of Alzheimer’s disease.
“This dysfunction in cell communication occurs at a very early stage in the before memory impairment is detectable,” said Jasmin Hefendehl, , the first author of the study. “This makes our discovery particularly interesting, as it opens a window for an early intervention strategy to possibly prevent or delay neuron and memory loss.”
Story Source: The above story is based on materials provided by ALZHEIMERSNEWSTODAY
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