The study published on Wednesday in the Journal of Experimental Medicine, showed that an enzyme called BACE1 facilitates the formation of amyloid plaques in the brains of mice with this neurodegenerative disease.
One of the earliest events in Alzheimer's disease was an abnormal build-up of beta-amyloid peptide, which could form large, amyloid plaques in the brain and disrupted the function of neuronal synapses.
Researchers found that the enzyme helped produce beta-amyloid peptide by cleaving amyloid precursor protein (APP), Xinhua reported.
Therefore, drugs that inhibit BACE1 are being developed as potential Alzheimer's disease treatments but, because BACE1 controls many important processes by cleaving proteins other than APP, these drugs could have serious side effects.
Yan Riqiang and colleagues from the Cleveland Clinic Lerner Research Institute generated mice that gradually lost this enzyme as they grew older.
These mice developed normally and appeared to remain perfectly healthy over time.
"To our knowledge, this is the first observation of such a dramatic reversal of amyloid deposition in any study of Alzheimer's disease mouse models," Yan was quoted as saying.
Decreasing BACE1 activity also resulted in lower beta-amyloid peptide levels and reversed other hallmarks of Alzheimer's disease, such as the activation of microglial cells and the formation of abnormal neuronal processes.
Loss of BACE1 also improved the learning and memory of mice with Alzheimer's disease.
It has raised hopes that drugs targeting this enzyme will be able to successfully treat Alzheimer's disease in humans.
"Our study provides genetic evidence that preformed amyloid deposition can be completely reversed after sequential and increased deletion of BACE1 in the adult," said Yan.
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