BACE Inhibitor Improves Function in Mouse Models of Alzheimer’s Disease

BACE Inhibitor Improves Function in Mouse Models of Alzheimer’s Disease
A recent study in mice showed that BACE inhibitors not only reduce cerebral amyloid-beta (Aβ) levels, but they also may improve the neural circuit and memory impairments in patients with Alzheimer’s disease. Researchers now plan to conduct a large-scale clinical trial with about 1,000 patients to determine in the unexpected and encouraging results found in mouse models can be replicated in humans. The study titled, “BACE inhibition-dependent repair of Alzheimer’s pathophysiology,” was published in the journal Proceedings of the National Academy of Sciences of the United States of America. "What really impressed and amazed us was the reversibility of the symptoms," said Aylin Keskin, lead author of the publication. "Before the treatment, the mice had a marked clinical picture with amyloid beta plaques in their brain. Nevertheless, the substance was able to restore important brain functions and abilities." The presence of Aβ plaques is a major characteristic of the brains of Alzheimer’s disease patients. Aβ is produced through the work of a key enzyme called β-secretase BACE, and inhibitors for this particular enzyme are currently being used to treat Alzheimer’s disease in clinical trials. The basic hypothesis behind the manifestation of Alzheimer’s disease is that the abnormal accumulation of Aβ plaques in the brain leads to neuronal dysfunction and eventually memory impairment. However, experiments conducted with other substances, such as antibodies against Aβ plaques, have shown variable results in terms of restoring neuronal function. Therefore, researchers at Technical
Subscribe or to access all post and page content.


  1. On new Base Inhibitor study, please send me information, news, and clinical trial information. Also send news the 1000 people that are applying for this clinical trial. I was in the Merc MK 8931 mild to moderate base inhibitor trisl phase 3 and they discontinued it telling us it was ineffective.
    If there’s new basevinhititir trial that’s promising, I want to be included.

  2. Eliseo Martinez says:

    Before clinical trials how about verifying with a duplicate study? Or concurrently. So much effort on amyloid is taking away talent that should be looking upstream at the genome, factors such as the role of histone misfolding and kyneuronins.

Leave a Comment

Your email address will not be published. Required fields are marked *