New Experimental Drug Reverses Symptoms of Dementia

Alzheimer's disease affects a significant percentage of adults older than 65. It is the most prevalent form of dementia worldwide and is increasingly present in developed countries, where the lifespan is increasing. Medical science urgently seeks solutions to prevent or slow down the progression of Alzheimer's in old age. Currently, there is no reliable method to prevent or treat Alzheimer's other than avoiding some known risk factors.

Although the causes of the disease remain poorly understood, an important aspect of its neuropathology is now well-documented - the onset of Alzheimer's is closely related to the proliferation of senile plaques in the brain. Senile plaques are deposits of amyloid beta that seem to disrupt normal neurological activity. The brains of Alzheimer's patients have abnormally high amounts of these deposits. Therefore, there is ongoing research to find substances or drugs that decrease the production of these senile plaques.

BACE inhibitor drugs show promise


This is what the scientists at the Technical University of Munich seem to have achieved. They recently released the results of a study in which a BACE inhibitor was administered to mice exhibiting symptoms of dementia. BACE inhibitors are a new class of drugs that target the enzyme responsible for the production of amyloid beta, beta-secretase. Scientists believe that these drugs hold promise for the treatment or prevention of Alzheimer's in the future given the mechanism of their action.

In this study, scientists administered the drug to mice through food for eight weeks. When they looked for the effects of this drug they observed that the amount of amyloid beta in the brains of the mice had decreased. More importantly, there were also clear cognitive and behavioral improvements in the animals after the drug treatment. Memory, one of the most affected functions in Alzheimer's patients, showed solid improvement.

Using two-photon microscopy, Aylin Keskin "lead author" and colleagues found that the brains of the mice after the treatment had lower amounts of hyperactive neurons (another Alzheimer's biomarker). And the slow-waves patterns also reverted to healthy patterns. The promising results of this study have granted the TUM team the opportunity to perform a large-scale clinical trial on humans in the near future. They expect to experiment the drug on at least one thousand Alzheimer's patients.

Another positive outcome from this study is a clearer picture of how exactly amyloid beta plaques affect the neurological functions in the brain. This data is an important addition to the current understanding of Alzheimer's etiology. If the human trials show similar treatment success, this drug could be the precursor to the first effective treatment for Alzheimer's.