Published: Sat, February 17, 2018
Health Care | By Oscar Goodwin

New study reverses Alzheimer's in mice, while similar big clinical trial fails

New study reverses Alzheimer's in mice, while similar big clinical trial fails

The weaning off of BACE1 activity also led to improved learning and memory in mice with Alzheimer's disease. Merck is yet to share data from the second phase 3 trial but the take-home message from the early stoppage is clear: Verubecestat is as ineffective in prodromal Alzheimer's as it is in mild to moderate forms of the disease.

The discovery means drugs targeting this enzyme could be effective in reversing the effects of Alzheimer's, although at present, drugs doing this could have serious side-effects, as APP is not the only protein that would be inhibited.

The offspring also started forming amyloid plaques at 75 days old, even though their BACE1 levels were half that of normal mice.

WEDNESDAY, Feb. 14, 2018 (HealthDay News) - Sustained and increasing BACE1 inhibition can reverse amyloid deposition in a mouse model of Alzheimer's disease (AD), according to a study published online Feb. 14 in the Journal of Experimental Medicine.

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A number of drugs have already been developed as potential ways to inhibit BACE1, and therefore stop amyloid plaques from forming, but the problem is the enzyme also controls a range of important cleaving processes.

Amyloid plaques are believed to contribute to Alzheimer's disease because the sticky clumps could interfere with communications between brain synapses. Cut out BACE1 completely and the brain's functionality will be seriously damaged. Earlier studies showed that mice with no BACE1 had severe problems in their neurodevelopment so the experiment was set up to glean whether adults would be less negatively affected by reduced levels of the enzyme.

To investigate whether inhibiting BACE1 in adults might be less harmful, Riqiang Yan and colleagues generated mice that gradually lose this enzyme as they grow older.

Meanwhile, Amgen and Novartis are testing a BACE inhibitor known as CNP520, which they are testing on people at-risk of Alzheimer's, to see if it could work preventatively.

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"When we looked at the mice later - at six months old and 10 months old - all those pre-existing plaques were gone", Yan told the Chicago Tribune. These hallmarks of Alzheimer's disease have been reversed (right) in animals that have gradually lost the BACE1 enzyme. Closer inspection of neuronal activity did reveal that reducing BACE1 activity did not completely restore synaptic functions and the researchers do suggest that caution is still warranted as the enzyme does seem to be fundamental for optimal cognitive function.

"This new study adds to findings that suggest this approach is a promising avenue for future therapies, but drugs that target this protein are yet to show any benefit to people with Alzheimer's in clinical trials".

BACE1 functionality looks to be a hard balance to strike, but the hope is that further research can be done to pinpoint the ideal levels of the troublesome enzyme.

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