Researchers make important step towards novel Alzheimer's disease therapeutic

New compound is able to stop the formation of amyloid plaques in a transgenic mouse model for Alzheimer's disease

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Dec 11, 2015
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A team of researchers, based in the Republic of Korea, from GoshenBiotech Inc. and the Korea University of Science and Technology, has discovered a novel compound capable of causing disaggregation of amyloid-β (Aβ) oligomers and plaques, which may have potential as a therapeutic for Alzheimer's disease (AD).

AD is characterized by the transition of Aβ monomers into toxic oligomers and plaques. Bearing in mind that Aβ abnormality typically precedes the development of clinical symptoms, it is conjectured that an agent capable of disaggregating existing Aβ aggregates may be an effective treatment for AD.

“There is currently a strong focus on developing treatments for Alzheimer's that aim to stop the build-up of the hallmark Alzheimer's protein, amyloid, in the brain,” commented Simon Ridley, Director of Research at Alzheimer's Research UK, in a recent press release. "Although some anti-amyloid drugs are currently in late-stage clinical testing, several trials have also failed and there is much debate as whether this is a suitable approach for a new treatment. Many of the current drugs being explored act to stop the formation of amyloid plaques in the brain which mean they may need to be given early in the disease process."

In a previous study, the research group at the Korea University of Science and Technology had discovered a set of molecules that could either accelerate or slow down the formation of amyloid plaques in vitro. In their latest study, they explored the effect of one of these compounds – 4-(2-hydroxyethyl)-1-piperazinepropanesulphonic acid (EPPS) – in transgenic mice, developed to exhibit features of AD.

The group reported that, when administered orally, EPPS was found to substantially reduce hippocampus-dependent behavioral deficits, brain Aβ oligomer and plaque deposits, glial γ-aminobutyric acid (GABA) release and brain inflammation in an Aβ-overexpressing, APP/PS1 transgenic mouse model. Based on their observations, the team concluded that the ability of EPPS to rescue Aβ aggregation and behavioral deficits provides compelling evidence to support the theory that Aβ accumulation is an important mechanism underlying AD.

"With no new treatments for Alzheimer's licensed since 2002, we urgently need to capitalize on promising early science to make sure it's progressed as quickly as possible towards clinical testing," said Ridley. The discovery of EPPS is a promising step towards the development of novel AD therapeutic agents.

Sources:

Kim HY,Kim HV,Jo S et al. EPPS rescues hippocampus-dependent cognitive deficits in APP/PS1 mice by disaggregation of amyloid-β oligomers and plaques. Nat. Commun. 6, 8997 (2015).

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Go to the profile of Hannah Coaker

Hannah Coaker

Contributor, Future Science Group

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