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Alzheimer's disease (AD) was firstly described and named after a psychiatrist and pathologist Dr. Alois Alzheimer in 1906. It is an irreversible, progressive brain disorder that affects cognitive functions. Symptoms usually starts in patients’ mid-60s, but can also occur earlier. According to estimated, 5 million people in the USA have the disease, for which currently there are no treatments to stop or reverse the progression. Exiting therapies only temporarily improve symptoms. Its incidence is rising in line with the aging population. Mechanisms of AD have yet completely understood.

Published 26 April 2017 in Alzheimer’s Research and Therapy, a new study, carried out by Doris Lambracht-Washington, Min Fu, Pat Frost and Roger Rosenberg at UT Southwestern Medical Center, now reports a DNA vaccine that could protect against toxic proteins associated with AD. The researchers demonstrated that a DNA Aβ42 trimer vaccine led to high levels of antibody responses in rhesus macaques.

The accumulation of amyloid plaques between neurons in the brain is one of the markers of AD. This study showed that a vaccine that contains DNA of the toxic beta-amyloid (Aβ) protein can elicit a protective immune response. In the study, 6 rhesus monkeys received two different doses of the DNA Aβ42 trimer vaccine. The researchers monitored the humoral and cellular immune response in the animals. Results showed that the vaccine triggered high titer antibody responses (anti-Aβ42 IgG and IgA antibodies) in the monkeys. Moreover, these antibodies were able to detect amyloid plaques in the brain of an AD mouse model. Importantly, the vaccine did not accompany inflammatory interferon (IFN)-γ- and interleukin (IL)-17-producing T-cell responses. The researchers hope that their vaccine has protective effects in patients with early AD. (Cusabio produces and offers FITC conjugated antibody.)

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