Scientists reverse Alzheimer's disease in mouse model

Scientists reverse Alzheimer's disease in mouse model

Meanwhile, the animals' learning and memory improved. An excessive accumulation of this peptide eventually leads to the Alzheimer's-related brain pathologies known as beta-amyloid plaques.

Verubecestat is a small molecule inhibitor of the beta-site amyloid precursor protein cleaving enzyme (BACE1).

Dr Riqiang Yan, of the Cleveland Clinic Lerner Research Institute in the U.S., said: "To our knowledge, this is the first observation of such a dramatic reversal of amyloid deposition in any study of Alzheimer's disease mouse models".

The research found that slowly depleting the presence of a certain enzyme can reverse the formation of amyloid plaques in the brain.

We still may be some years away from an effective Alzheimer's disease treatment, but all is certainly not lost with many dedicated researchers still working hard to find potentially useful drug targets. Therefore, inhibiting it may cause some impairments as a side effect.

Just hours before this latest Cleveland Clinic Lerner Research Institute study was published, another blow to the field came when Merck announced it was discontinuing a Phase 3 clinical trial into a drug called verubecestat, following a recommendation suggesting, "it was unlikely that positive benefit/risk could be established if the trial continued". The team from the Cleveland Clinic Lerner Research Institute in the USA detailed the findings in the Journal of Experimental Medicine.

Why Traders Are Chasing Duke Realty Corporation (DRE), HB Fuller Company (FUL)
Forbes J M Llp reported 0.09% stake. 779.91 million shares or 1.33% less from 790.40 million shares in 2017Q2 were reported. The fund owned 68,950 shares of the real estate investment trust's stock after selling 112,900 shares during the period.

The results of this laboratory experiment have now been published in the Journal of Experimental Medicine. To their surprise, the mice developed normally and appeared to remain perfectly healthy over time. The scientists then proceeded to breed them with other rodents that had Alzheimer's-like symptoms, such as a buildup of amyloid plaque in the brain.

Eli Lilly also dropped the method in 2013, but a year later joined forces with AstraZeneca to try another version in early-stage patients, a similar age to the mice tested in Yan's new study.

It raises hopes that drugs targeting BACE1 could successfully treat the disease in humans.

However, the study also found that the functioning of the synapses - that is, the spaces between neurons that facilitate their communication - was only partially restored.

The findings could be a game changer for the pharmaceutical industry, which has had a rough ride with BACE1 inhibitors - although some analysts claim Merck's failure suggests we are barking up the wrong tree. "Future studies should develop strategies to minimize synaptic deficiency resulting from significant inhibition of BACE1 to achieve maximum and optimal benefits for patients with Alzheimer's", says Yan.

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