Researchers from The University of Texas at Austin and the University of Illinois at Urbana-Champaign have identified a potential link between brain iron levels and Alzheimer’s disease using a new imaging probe. This technique reveals that, in areas of the brain affected by amyloid beta plaques, there is also an increase in reactive iron species, specifically Fe2+ and Fe3+. This finding suggests that iron redox changes may be significant in the development or progression of Alzheimer’s.
The study introduced DNA-based fluorescent sensors capable of simultaneously detecting both forms of iron and indicating their quantities and distribution in brain tissues, a first for such imaging methods. Understanding the relationship between elevated iron ratios and amyloid plaques could illuminate mechanisms of cell death in Alzheimer’s. Researchers plan further investigations in genetically modified Alzheimer’s mouse models to clarify whether these iron changes contribute directly to cell death or are merely byproducts.
If established that iron redox is a causal factor, strategies to develop drugs aimed at altering the Fe2+/Fe3+ ratio could emerge, potentially offering new therapeutic routes for protecting brain cells from Alzheimer’s-related damage.
