Can Ultra-Processed Foods Accelerate Brain Aging?

New research co-authored by Targeting Mitochondria 2026 speaker Benedict C. Albensi examines how ultra-processed foods may influence cognitive decline, neuroinflammation and mitochondrial bioenergetics.

What we eat may influence how our brain ages.

A major review published in the Annual Review of Nutrition in August 2026 examines the growing body of evidence connecting ultra-processed food consumption with brain ageing, cognitive decline and neurodegenerative disease. The work brings together experimental and clinical evidence and explores multiple biological pathways that could connect diet to the ageing brain.

One of the co-authors is Prof. Benedict C. Albensi, Associate Dean of Research and Professor at Nova Southeastern University and a confirmed speaker at Targeting Mitochondria 2026 in Berlin. Albensi has also played a leadership role within the Alzheimer's Association ISTAART Nutrition, Metabolism and Dementia community.

The study has now moved beyond the scientific literature: on September 24, Newsweek highlighted the work in an article examining what ultra-processed foods may be doing to the ageing brain.

From food processing to mitochondrial bioenergetics

The review describes a network of potential mechanisms rather than a single pathway: metabolic dysfunction, insulin resistance, gut dysbiosis, oxidative stress, immune activation, disruption of the blood-brain barrier and neuroinflammation.

Importantly for the World Mitochondria Society, the review also examines mitochondrial bioenergetics. Experimental evidence discussed by the authors links dietary patterns associated with highly processed foods with increased oxidative stress and alterations in mitochondrial electron-transport-chain complexes in the brain. The authors emphasize that much of the mechanistic evidence still comes from experimental models and that stronger human mechanistic studies are needed.

This raises a broader question:

Could diet progressively reduce the energetic resilience of the ageing brain, making neurons more vulnerable to neurodegeneration?

That question connects directly with the perspective Prof. Albensi will bring to Targeting Mitochondria 2026.

In Berlin: Is Alzheimer’s disease first a disorder of mitochondrial resilience?

At Targeting Mitochondria 2026, Prof. Albensi will present:

“Is Alzheimer’s Disease a Mitochondrial Resilience Disorder Before It Becomes a Proteinopathy?”

His lecture will explore whether mitochondrial dysfunction, declining bioenergetic capacity and neuroinflammation could emerge before the classical pathological manifestations of Alzheimer’s disease—and whether this could open new opportunities for earlier intervention.

From nutrition to metabolism, from mitochondrial resilience to neurodegeneration, understanding what happens before irreversible brain pathology develops may become one of the major challenges of precision medicine.

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