Drug Candidate Shows Promise For Easing Alzheimer's Symptoms

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A drug under development could potentially be used to treat Alzheimer’s and other neurocognitive diseases as it stops the combining of dangerous tau protein in the brain, based on experiments in mice.

Armen Giese, MD, Center for Neuropathology and Prion Research at the LMU Munich, Germany, and colleagues worked with mice treated to have a genetic defect that caused them to display various characteristics typical of tauopathies, such as aggregation of tau proteins and cognitive disorders.

In the case of Alzheimer's disease, the tau proteins are altered, become detached from microtubules and aggregate into tangles. This results in the impairment of the microtubules’ function and the cell's metabolism, leading to the death of neurons.

The mice were then given the drug, “anle138b,” which lead to an easing of disease symptoms and improvement in cognition, the researchers reported in the journal Acta Neuropathologica. The drug is given orally.

“In contrast to other substances, anle138b is orally available because of its chemical and metabolic characteristics. Therefore, it stays for hours within the body and targets specifically protein aggregation,” Christian Griesinger, PhD, of the Max Planck Institute for Biophysical Chemistry, Munich, said in a statement.

The researchers caution that the results of anle138b are not directly transferable to humans and will need clinical trials.

Drug Candidate Shows Promise For Easing Alzheimer's Symptoms
Anle138b, which is given orally, was shown to stop the angling of tau protein in the brains of mice.

Professor Armin Giese from the Center for Neuropathology and Prion Research at the LMU Munich and researchers at the Max Planck Institute for Biophysical Chemistry in Göttingen and at the German Center for Neurodegenerative Diseases (DZNE) in Bonn have analyzed a novel substance that could serve as a prototype for the development of drugs to treat Alzheimer's and other brain diseases. Known as "anle138b," this substance ameliorated disease symptoms in mice and improved their cognition.

Under normal conditions, the tau proteins stabilize the microtubules that are part of the cytoskeleton of neurons in the brain. The cytoskeleton gives the cell mechanical stability and serves as a transport network for substances essential to the cell's metabolism. However, in cases of Alzheimer's disease and other tauopathies, the tau proteins have undergone an alteration: they become detached from microtubules and aggregate into filamentous tau-tangles. As a result, the microtubules' function and the cell's metabolism are impaired, which eventually leads to neuronal death.

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