Sticky plaques of proteins called amyloids mark several different, though related degenerative brain diseases including Alzheimer’s, Parkinson’s, and the prion disease Creutzfeldt-Jakob. Symptoms of these disorders overlap but methods to diagnose and monitor them are not very advanced.
UC San Diego scientists have devised several new fluorescent probes that change color depending on what type of amyloid they encounter. Thus, one of the probes glows yellow when marking amyloid deposits associated with prion disease, and glows green when binding to amyloids associated with Alzheimer’s disease in tissue samples.
Because amyloids accumulate in the eye as well as the brain, the hope is that one day neurodegenerative diseases could be diagnosed with simple eye drops or ointment and an eye exam.
— Findings appear in the Journal of the American Chemical Society. More information at
Autoimmune response and artery wall inflammation
In addition to cholesterol, studies have demonstrated that inflammation plays a role in the plaque buildup (known as atherosclerosis) that is the underlying cause of most heart attacks and strokes. But knowledge of which immune cells are key to this process has been sketchy.
Now researchers at the La Jolla Institute for Allergy & Immunology report on the specific type of immune cells (CD4 T cells) that orchestrate the inflammatory attack on the artery wall. Further, researchers discovered that these immune cells, in mice models, behave as if they “memory” of the antigen that causes them to launch. This is an unexpected and fascinating discovery because it indicates an autoimmune component of heart disease in which the body mistakenly attacks normal cells.
Because immune memory is the underlying basis of successful vaccines, in theory, this finding offers the intriguing possibility of one day exploring the development of a vaccine for heart disease.
— The study is published in the Journal of Clinical Investigation. News release at
Copper and Prion disease
Prion diseases — also known as transmissible spongiform encephalopathies (TSEs) — are a family of rare progressive neurodegenerative disorders that affect both humans and animals (most famous example is “mad cow” disease) leading to progressive neurodegeneration and death.
The causative agents of TSEs are prions — abnormal, pathogenic agents able to induce abnormal folding of specific cellular proteins found in the brain. This abnormal protein folding leads to brain damage and the characteristic signs and symptoms of the disease.
For many years, researchers have known that prion proteins bind copper. But what wasn’t clear was whether this was a good thing or a bad thing relative to disease progression. Now scientists at The Scripps Research Institute have discovered, in mouse studies, that animals lacking a copper-transport gene living significantly longer when infected with a prion disease than did normal mice. Thus, reducing the body level of copper could delay the onset of prion disease.
— Findings appear in the Proceedings of the National Academy of Sciences. News release at
Lynne Friedmann is a science writer based in Solana Beach.