Many studies have reported elevated αA and αB‐crystallin expression in neurodegenerations, including ocular hypertension, animal models of uveitis, diabetes and optic nerve transection27, 37 and AMD,38 and Alzheimer's disease and Parkinson's disease,39, 40 suggesting they play a common role in neurodegenerations as an intrinsic protective response to damage. This evidence concerns the gene TEAD1 and early-onset autosomal dominant Alzheimer disease.