Recent research sheds light on specific ages when interventions to slow cognitive decline might be most effective due to changes in brain aging.
As individuals age, the brain undergoes significant changes, including neuron loss and brain shrinkage, which can lead to cognitive decline characterized by memory issues, slower thinking, and learning difficulties. Researchers, aiming to hinder age-related cognitive decline, explore various interventions, including medications, cognitive stimulation, and lifestyle adjustments involving diet and exercise.
A recent study published in the journal PNAS has identified specific ages where interventions may have increased efficacy. The study analyzed neuroimaging data from over 19,000 individuals across four datasets, such as the U.K. Biobank and Mayo Clinic Study of Aging. Scientists focused on how brain networks, or interconnected brain regions performing specific functions, change communication patterns as one ages. The study’s lead author, Lilianne R. Mujica-Parodi, PhD, highlights that these networks can be monitored using fMRI and EEG technologies.
The researchers discovered that brain networks degrade in a non-linear pattern with distinct transition points. Notably, the network degradation begins to manifest around age 44, accelerates sharply by age 67, and stabilizes by age 90. In physiological systems, the balance between energy demand and supply is crucial. Losing this balance stresses the system, leading to further disruption. Mujica-Parodi likened this to a city relying on steady electricity; a brief outage leaves no lasting harm, but prolonged outages lead to debilitating infrastructure damage.
Mujica-Parodi’s study suggests that in the 40s, diminished energy access initiates degeneration, which accelerates in the 60s and subsequently solidifies the degeneration path. Intervening early is akin to addressing minor issues before they escalate, as restoring a severely damaged system becomes more challenging.
Additionally, the study highlights aging brain networks’ primary driver as neuronal insulin resistance, influenced by the Alzheimer’s-related APOE protein and the insulin-responsive GLUT4 glucose transporter. Yet, the neuronal ketone transporter, MCT2, may offer protective advantages against this aging.
Neurons generally use glucose and ketones for energy. While glucose uptake in the brain via GLUT3 is common, regions using GLUT4 rely on insulin, now recognized as more significant in brain function than previously believed. Ketones, accessible even when glucose is unmetabolized due to insulin resistance, provide an alternative energy source, making the MCT2 transporter essential. This capability potentially protects the aging brain.
This study’s outcomes prompt questions about the ketogenic diet’s role in safeguarding aging brains. Verna Porter, MD, notes that utilizing ketones as an alternative fuel offers a promising prevention route against cognitive decline. Although intriguing, more studies are essential to ascertain the long-term viability of a ketogenic diet, particularly in those at risk for Alzheimer’s disease.
Gary Small, MD, also underscores the importance of early intervention in cognitive decline prevention and research backing the idea that midlife keto diets might mitigate late-life cognitive issues. He suggests that clinical trials on middle-aged volunteers could pioneer new prevention strategies.
This research underscores the potential of specific age windows for effective interventions against cognitive decline, emphasizing early intervention as a critical strategy.
