Reversing Alzheimer’s Disease May Be Possible, According To New Mouse Study


Written by lkods on February 19, 2018. Posted in Blog

As reported in ScienceDaily, one of the earliest events that occurs with Alzheimer's disease is an unusual buildup of beta-amyloid peptide, which then can form the characteristic amyloid plaques in the brain. These plaques disrupt the function of neuronal synapses. Beta-secretase (BACE1) is an enzyme that helps to produce the problematic beta-amyloid peptide.

A team of researchers from the Cleveland Clinic Lerner Research Institute have found that — in mice with Alzheimer's disease — gradually depleting the BACE1 enzyme completely reverses the formation of amyloid plaques in the brain. Not only that, but this reversal also led to improvements in the animals' cognitive function.

The new report, published this week in the Journal of Experimental Medicine, brings hope that scientists will be able to develop drugs that target this enzyme in a bid to find a successful treatment for Alzheimer's disease in people.

Testing BACE1 reduction in adult mice

BACE1 controls many important processes, so simply getting rid of the enzyme could have serious side effects. Mice completely lacking BACE1 have severe neurodevelopmental defects — but, researchers wondered, would inhibiting this enzyme in adults be less harmful?

To find out, the team of scientists generated mice that gradually lose the BACE1 enzyme as they age. These mice developed as expected and seemed to remain perfectly healthy throughout their lifespan. Next, the team bred these mice with a group of mice that begin to develop amyloid plaques and Alzheimers disease when they reach 75 days old. The resulting offspring formed plaques at the expected age, with BACE1 levels close to half what they would normally be at 75 days.

Incredibly, these plaques began to shrink and disappear as the mice continued aging (and as their BACE1 levels continued to fall). Even more remarkable, by the time these cross-bred mice reached 10 months of age, the plaques had entirely disappeared.

In addition, the lower BACE1 activity also led to lower beta-amyloid peptide levels and reversals in other benchmarks of Alzheimer's disease (like the activation of microglial cells and formation of abnormal neuronal processes). The memory of the mice with Alzheimers disease saw improvement with the loss of BACE1 — but the depletion of the enzyme only partially restored synaptic activity, which may point to BACE1 as necessary for optimal cognition.

More study is needed, but this groundbreaking research certainly suggests progress in identifying treatments for Alzheimers disease, something that has proved elusive thus far.

Further Reading & References

Xiangyou Hu, Brati Das, Hailong Hou, Wanxia He, Riqiang Yan. BACE1 deletion in the adult mouse reverses preformed amyloid deposition and improves cognitive functions. The Journal of Experimental Medicine, 2018; jem.20171831 DOI: 10.1084/jem.20171831

Rockefeller University Press. "Alzheimer's disease reversed in mouse model." ScienceDaily. ScienceDaily, 14 February 2018.

Alzheimer's Disease Reversed in Mouse Model." Genetic Engineering & Biotechnology News. 14 February 2018.

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