Mayo Clinic researchers identify key DNA changes in the brains of people with Alzheimer’s disease
Peer-Reviewed Publication
In honor of Alzheimer's Awareness Month, we’re exploring the science and stories surrounding Alzheimer’s disease.
Updates every hour. Last Updated: 21-Jun-2026 18:15 ET (21-Jun-2026 22:15 GMT/UTC)
Neurodegenerative disorders such as Alzheimer's disease (AD) are typically diagnosed after irreversible pathology has developed. Aging, the strongest risk factor, drives molecular changes that predispose the brain to synaptic dysfunction and proteinopathy (neurodegenerative diseases characterized by the abnormal folding, aggregation, and accumulation of specific proteins within neurons or brain tissues). Glycosylation and extracellular matrix (ECM) remodeling are processes crucial for protein folding, stability and cell signaling and represent underexplored mechanisms linking aging to neurodegeneration, opening avenues for biomarker discovery; yet mass spectrometry-based glycoproteomics and glycomics studies have remained limited until now.
Using a unique on-slide tissue digestion method and advanced mass spectrometry technique that captures substantially more molecular information than prior methods, researchers from Boston University Chobanian & Avedisian School of Medicine have discovered protein and sugar level changes that occur with aging and Alzheimer’s disease brains, especially when Alzheimer’s disease co-occurs with Lewy body pathology.
Researchers measured levels of the blood biomarker tau phosphorylated at threonine 217 (pTau217) in 429 participants whose amyloid pathology status had been characterized by PET scans.
An exploratory clinical trial from the University of Pittsburgh suggests that low‑dose oral lithium may help slow the decline of verbal memory, or ability to remember and recall words and sentences, in older adults with mild cognitive impairment, particularly among those with evidence of amyloid beta—one of the hallmark biomarkers of Alzheimer’s disease.
A new culprit: While billions of dollars have been spent targeting Amyloid beta (Aβ) in Alzheimer’s patients, a newly reevaluated, shorter peptide known as P3 forms toxic clumps faster than Aβ and may also contribute to the disease.
Explaining stalled progress: The overwhelming focus on Aβ, and the erroneous assumption that P3 is harmless and water-soluble, may explain why current Alzheimer’s treatments show limited success and fail to stop the disease’s progression.