Hopes of reversing Alzheimer's raised by enzyme study

Hopes of reversing Alzheimer's raised by enzyme study

This was not the only sign of Alzheimer's that the enzyme loss helped to reverse: the mice's levels of beta-amyloid peptide also dropped, and microglia - brain cells that, when activated, had previously correlated with amyloid plaque density - were now deactivated.

Noting that BACE1 initiates the generation of the β-amyloid peptide, Xiangyou Hu, Ph.D., from the Cleveland Clinic, and colleagues generated conditional knockout BACE1 mice and bred them with ubiquitin-Cre mice to induce BACE1 deletion after early developmental stages.

They claim their tests on a 20-month-old mouse - equivalent to a 50-year-old human - show it could be possible to halt the disease if it is caught decades earlier than usual.

The data shows that BACE1 inhibitors "have the potential to treat patients with Alzheimer's and without unwanted toxicity".

Already aware of the Merck failure, Yan told Daily Mail Online last night that he still believes BACE1 is the answer to preventing and treating Alzheimer's.

In fact, mice that lack the enzyme completely suffer from severe deficits of neurological development.

Verubecestat belongs to a class of experimental Alzheimer's drugs called BACE1 inhibitors that target an enzyme involved in the formation of the toxic amyloid protein that turns into plaques in the brains of Alzheimer's patients.

The researchers were led by Riqiang Yan, of the Department of Neuroscience at the University of Connecticut School of Medicine in Farmington.


A new study has successfully reversed both the biological and behavioral hallmarks of Alzheimer's disease in mouse models.

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.

These mice developed normally and appeared to remain perfectly healthy over time.

Also, these neuronal changes were reflected in the mice's memory and learning abilities, which also improved. Therefore, inhibiting it may cause some impairments as a side effect. This suggested to the researchers that some BACE1 may be needed for synaptic health.

On Tuesday, Merck announced in a statement that it has pulled the plug on a trial with patients given either a placebo, or 12mg or 40mg of verubecestat, once a day.

Scientists also used brain imaging to measure the functionality of each patient's white matter. That is now in phase 3 clinical trials.

But the once-exciting trial has slowly spluttered to a halt: the firm shelved a similar trial of the same drug Verubecestat in late-stage patients a year ago, but had hoped it could work in early or mid-stage sufferers.

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