This is another paper using light for targeting β-amyloid in Alzheimer disease with light in a very interesting strategy. It's known that it's possible to desegregate β-amyloid with near-infrared light. The scientists from China start from the premises that UV could be used to successfully target β-amyloid. Indeed UV does not penetrate past a few millimetres under skin, so there is no hope to reach the brain where resides much β-amyloid plaques.
Yet Mengmeng Ma and colleagues observed that there is no need to reach the brain, as removing β-amyloid in the blood stream makes it been removed from the brain. It's a phenomenon called "Peripheral clearance".
While β-amyloid deposition is located in the brain in Alzheimer disease, peripheral clearance of β-amyloid may possibly also lower brain levels. The kidney, the skin, the gastrointestinal tract, and the liver contribute to peripheral β-amyloid clearance. β-amyloid could be detected in urine of humans. Recent evidence suggested that hepatic clearance of β-amyloid is impaired in liver cirrhosis. There is some evidence that patients with chronic liver diseases have an increased risk for Alzheimer disease.
So it the idea that targeting β-amyloid on a peripheral artery is very attractive. But indeed the scientists from China could not use UV light to target any large artery because its very low penetrance. So they used a proxy: An engineered peptide which when illuminated with IR, restitues this energy as UV.
The authors say that was useful in a mice model of Alzheimer. Indeed this must be taken with a grain of salt as 1. desegregation of β-amyloid plaques seems to have no impact on Alzheimer disease in humans and 2. successful trials on mice models of neurodegenerative diseases are rarely successful on humans.
Nevertheless it's a very interesting article exploring new ideas.
