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 University of Munich set out to determine the relationship between Aβ plaques and the disease pathology of Alzheimer’s. Their study made use of a new compound t