Research conducted at the National University of Singapore has revealed that a naturally occurring aging molecule may enhance memory functions impaired by Alzheimer’s disease. The study, published on January 25, 2026, in the journal Aging Cell, identifies calcium alpha-ketoglutarate (CaAKG) as a potential treatment that could restore vital memory processes in the brain.
Led by Professor Brian K Kennedy from the Yong Loo Lin School of Medicine, the research explores how CaAKG can improve communication between brain cells. This compound, which declines with age, has shown promise in restoring early memory abilities that are typically affected first in Alzheimer’s patients. The findings suggest a safer approach to safeguarding brain health by utilizing a molecule that already exists within the body.
The study aims to shift the focus of Alzheimer’s treatment from merely addressing symptoms to exploring geroprotective strategies. These strategies target the biological processes of aging that contribute to various age-related conditions, including neurodegenerative diseases.
CaAKG Restores Memory Functions
Professor Kennedy expressed enthusiasm about the potential of CaAKG, stating, “Our findings reveal the exciting potential of longevity compounds in addressing Alzheimer’s disease.” He emphasized that compounds like CaAKG could complement existing treatment methods, potentially slowing memory loss and supporting brain health as individuals age.
The research demonstrated that CaAKG improves synaptic plasticity in models of Alzheimer’s disease. This means it enhances the way neurons communicate, restoring weakened signaling pathways and helping to repair associative memory, a critical cognitive function often lost early in the disease.
The team focused on long-term potentiation (LTP), a process essential for learning and memory formation. In Alzheimer’s disease, LTP is severely disrupted, leading to memory loss. The study found that CaAKG effectively restored LTP to normal levels, indicating its potential to support cognitive functions.
Mechanisms Behind CaAKG’s Benefits
The researchers also noted that CaAKG increases autophagy, the brain’s self-cleaning mechanism, which eliminates damaged proteins and supports neuron health. The molecule works through a newly identified pathway, activating L-type calcium channels and calcium-permeable AMPA receptors while avoiding NMDA receptors often impaired by amyloid plaque accumulation.
Additionally, CaAKG was found to restore synaptic tagging and capture, a mechanism that helps the brain link experiences and form memories. This capability suggests that CaAKG could enhance not only basic memory functions but also more complex learning abilities that decline in Alzheimer’s patients.
Dr. Sheeja Navakkode, the study’s first author, highlighted the significance of the research: “Understanding the cellular mechanisms of how CaAKG improves synaptic plasticity sheds light on new ways to protect memory and slow brain aging.” The implications of this study are profound, offering hope for developing treatments that may significantly improve the quality of life for those affected by Alzheimer’s disease.
The findings from the Yong Loo Lin School of Medicine advance the understanding of aging and its impact on cognitive health, positioning CaAKG as a key player in future therapeutic strategies aimed at enhancing memory and supporting healthy brain aging.
