Scientists Discover Breakthrough in Memory Research, Potential Treatment for Alzheimer’s
Scientists at the University of Colorado Anschutz Medical Campus have made a groundbreaking discovery in memory research that could lead to innovative treatments for Alzheimer’s disease and other neurological conditions. The study, recently published in the journal Nature, reveals that learning and memory rely on the structural functions of the CaMKII enzyme, rather than its enzymatic actions.
For over three decades, researchers believed that the enzymatic actions of the CaMKII enzyme, known as long-term potentiation (LTP), were crucial for learning and memory. However, the team of researchers, led by Ulli Bayer, Ph.D., professor of pharmacology at the University of Colorado School of Medicine, found that LTP requires the structural functions, not enzymatic actions, of CaMKII.
This discovery is significant because it opens the door to the development of a new class of inhibitors that specifically target the enzymatic activity of CaMKII, without affecting the structural functions necessary for memory and learning. Previous studies by Bayer’s laboratory showed that inhibiting CaMKII activity protected against the effects of amyloid-beta plaques, a hallmark of Alzheimer’s disease, without impairing LTP.
“This is super novel, as it has previously been thought that any CaMKII activity inhibitor would block synaptic plasticity that underlies learning and memory, so their chronic use would be counter-indicated,” said Bayer.
The potential use of these inhibitors in the treatment of brain conditions, including Alzheimer’s disease, could provide additional benefits in conjunction with current treatment strategies. While not claiming to be curative, the inhibitors have the potential to alleviate some of the most devastating symptoms of memory loss and learning.
The Bayer lab is now testing whether their findings can be applied for human therapy. If successful, this breakthrough could lead to innovative treatments for Alzheimer’s and other neurological conditions, offering hope for individuals and families affected by these diseases.
Reference:
“LTP induction by structural rather than enzymatic functions of CaMKII” by Jonathan E. Tullis, Matthew E. Larsen, Nicole L. Rumian, Ronald K. Freund, Emma E. Boxer, Carolyn Nicole Brown, Steven J. Coultrap, Howard Schulman, Jason Aoto, Mark L. Dell’Acqua and K. Ulrich Bayer, 30 August 2023, Nature.
DOI: 10.1038/s41586-023-06465-y