In a study led by Naruhiko Sahara from the department of functional brain imaging at the National Institutes for Quantum Science and Technology in Japan, researchers deleted or knocked out the p62 gene in mice with dementia, so they did not express p62 receptor proteins.

Using immunostaining and comparative biochemical analyses, the researchers found neurotoxic tau protein aggregates in the hippocampus and brainstem of p62 knockout mice. MRI scans showed the hippocampus of p62 knockout mice was atrophied and inflamed. A postmortem assessment revealed a greater loss of neurons in their hippocampus. Further immunofluorescent studies showed the abnormal tau species aggregates could cause cytotoxicity, which can lead to inflammation and neuron cell death in p62 knockout mice. Oligomeric tau, in particular, accumulated more in the brains of p62 knockout mice.

Combined imaging approach gives detailed picture of blood vessels
Mapping out the intricate network of blood vessels in tissues can help researchers to better understand the changes in diseases like dementia or cancer....

Atlas finds hundreds of genes that control the brain's shape
The shapes of our brains are heavily influenced by our genes, although the precise nature of this complex relationship is difficult to pin down. Now,...

New gene therapy could be effective in treating complex polygenic conditions
Scientists are applying gene therapy approaches in a new way by simultaneously administering a combination of cargos to treat complex polygenic neurodegenerative...