Scientists map the first step in Alzheimer’s protein aggregation and discover clues for future therapies
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: 30-Oct-2025 10:11 ET (30-Oct-2025 14:11 GMT/UTC)
A protein produced by the pathogenic bacteria Helicobacter pylori can block amyloid proteins from clustering, new research finds. The protein, called CagA, stopped other infectious bacteria from creating protective, amyloid-dependent biofilms – and also prevented the assembly of amyloids tied to Alzheimer’s disease, Parkinson’s disease, and Type 2 diabetes. “H. pylori has broader systemic effects that extend well beyond its traditional association with gastrointestinal disorders,” Zhen Jin and colleagues write. “These findings […] open up new avenues for exploring microbial components in the development of treatments for protein misfolding diseases.” Amyloid fibrils contribute to neurodegenerative disorders and Type 2 diabetes. Amyloids also compose the backbones of biofilms that bacteria make to evade the gut’s antimicrobial defenses. The bacterial species H. pylori secretes a protein named CagA that is known to help it compete against other bacteria. Yet, the mechanism by which CagA disrupts other microbes was unknown until now. While exposing various bacteria in the Pseudomonas genus to H. pylori-derived CagA, Jin et al. found that CagA prevents aggregation of a broad range of amyloid substrates. Further tests confirmed that CagA also deterred dysfunctional accumulation of Alzheimer’s disease-associated proteins, including tau and two forms of amyloid-beta (Aβ). CagA similarly limited clustering of α-synuclein, a protein implicated in Parkinson’s disease, and islet polypeptide, which plays a role in Type 2 diabetes.
Inspired by advances in cancer therapy, a team at the Buck Institute has engineered immune cells equipped with specialized targeting devices called chimeric antigen receptors (CARs) that can distinguish and respond to tau tangles and various forms of toxic amyloid plaques, both of which are implicated in Alzheimer’s disease pathology. The proof-of-concept study, now online at the Journal of Translational Medicine, holds the promise of being able to precisely deliver therapeutic drugs directly to affected areas of the brain with fewer side effects.
When it comes to advanced cancer or Alzheimer’s disease, over half of doctors would consider assisted dying for themselves, but preferences seem to vary according to their jurisdiction’s legislation on euthanasia, reveal the results of an international survey, published online in the Journal of Medical Ethics. And most say they would prefer symptom relief rather than life sustaining treatment for their own end of life care, indicate the responses.
Stanford PhD graduate Sophia Shi reveals groundbreaking research showing how protective sugar coatings on brain blood vessels deteriorate with age, contributing to cognitive decline. Her Nature publication demonstrates that restoring these critical molecules in aged mice significantly improves brain barrier function and cognitive performance, offering unprecedented hope for neurodegenerative disease treatment.