Researchers at the Djavad Mowafaghian Centre for Brain Health, in collaboration with scientists at the Chongqing Medical University in Chongqing, China, recently discovered a way to slow the deterioration of memory. These findings significantly advance our understanding of the mechanism by which memory in our brain decays, and are the first to establish an opportunity for intervention to slow the progression of Alzheimer’s disease (AD) and related dementias.

According to a paper recently published in the Journal of Clinical Investigation, inhibiting the removal of a subtype glutamate receptor from neuronal membrane surface, a process that causes memory loss, can rescue damaged cells and prevent further loss in AD models.

Slowing cognitive decline

“This is the first time we’ve been able to slow the progression of memory loss in AD,” says Dr. Weihong Song, co-author of the paper and the Canada Research Chair in Alzheimer’s Disease. “This is fantastic, because we’re seeing that the peptides discovered by Dr. Yu Tian Wang, the principal scientist of the study, can protect the brain from loss of long-term memory.”

Alzheimer’s disease is characterized by gradual loss of both short- and long-term memory. This new study from Dr. Yu Tian Wang and Dr. Weihong Song, together with leading authors Drs. Zhifang Dong and Tingyu Li of Chongqing Medical University, is not only the first to reveal the mechanism of memory decay, but also develops a specific intervention to slow down the memory decay under both physiological and pathological conditions.

Next steps

“This discovery is promising in terms of treatment and prevention – we are hopeful for the potential for new drug treatment to emerge out of these findings,” says Dr. Song. “Our next step is – we hope – to apply these findings to a small clinical trial.”

Neuritic plaques are a unique feature of AD and their main components are neurotoxic protein called Amyloid beta protein (Aβ). It is not yet well understood how Aβ forms neuritic plaques in brains and triggers neuronal death. “A better understanding of the hows and whys of these proteins leading to cognitive impairments will help us with some of our unanswered questions,” says Dr. Song.

Citation

Zhifang Dong, Huili Han, Hongjie Li, Yanrui Bai, Wei Wang, Man Tu, Yan Peng, Limin Zhou, Wenting He, Xiaobin Wu, Tao Tan, Mingjing Liu, Xiaoyan Wu, Weihui Zhou, Wuyang Jin, Shu Zhang, Todd Charlton Sacktor, Tingyu Li, Weihong Song, and Yu Tian Wang. Long-term potentiation decay and memory loss are mediated by AMPAR endocytosis. J Clin Invest. 2014. doi:10.1172/JCI77888.