One of the most widespread types of dementia, Alzheimer’s disease, causes slow neuronal damage and brain tissue death. Currently, researchers believe that genetic disorders and the accumulation of harmful damaged proteins of a certain type are what provoke the symptoms of memory loss and logic impairment.
Neuroscientists at the NYU Grossman School of Medicine revealed on Tuesday a new treatment to slow the progression of Alzheimer’s disease. The experiment involved elderly squirrel monkeys who had been diagnosed with Alzheimer’s.
According to the release, the proposed treatment prompted the immune system to absorb the toxic deformed fibril-forming proteins, also known as amyloid betas. The accumulation of these elements in the brain leads to the development of dementia.
The drug was described as “a class of innate immune regulators,” CpG oligodeoxynucleotides (CpG ODN), administered with a technique called “pulsing” used to prevent excess inflammation.
The tests showed that the group of elderly animals which received the drug had 59% fewer toxic amyloid beta plaque deposits compared with a control group that received no therapy, the researchers said. The compound was also said to improve cognitive function as treated animals appeared to absorb new information more quickly.
Earlier attempts at treatment aimed at the immune system have been unsuccessful – the drugs stimulated the immune system too much, causing dangerous levels of inflammation that could damage and destroy brain cells.
Scientist are now determined to test younger monkeys with less acute dementia symptoms.