Publication date: Oct 03, 2019
This post was originally published on this site Increasing the levels of a natural enzyme called nicotinamide mononucleotide adenylyltransferase – or Nmnat – halts the formation of mutant huntingtin (Htt) protein aggregates that build up in nerves cells in Huntington’s disease, a fruit fly study shows. -We discovered the neuroprotective role of a cellular ‘housekeeping’ enzyme in alleviating disease progression,” R. Grace Zhai, PhD, associate professor of molecular and cellular pharmacology at the University of Miami Miller School of Medicine and the study’s lead author, said in a press release. Huntington’s disease is characterized by mutations in the HTT gene, which results in the abnormal production and accumulation of mutated forms of the huntingtin (HTT) protein inside nerve cells, ultimately causing them to die. To learn more, researchers at the University of Miami Miller School of Medicine used a fruit fly model of Huntington’s disease with many characteristics that resemble those found in the human brain. Importantly, when the researchers engineered flies to express Nmnat only after the onset of Huntington’s disease, it significantly delayed the progression of neurodegeneration – -revealing the therapeutic potential of Nmnat-mediated neuroprotection at advanced stages of [the disease],” they said. -Our next step will involve screening drugs and compounds that could potentially increase Nmnat or enhance its ability to reduce the Htt aggregations that build up in Huntington’s disease,” Zhai said.
- Nmnat restores neuronal integrity by neutralizing mutant Huntingtin aggregate-induced progressive toxicity.