Furthermore, laminin is linked to modification of APP and Aβ processing and found in senile plaques in Alzheimer's Disease,66 where it prevents Aβ fibril formation and reduces neurotoxicity.32 This effect was confirmed in vivo, with laminin depletion accelerating Aβ-induced neurotoxicity, altering the distribution of Aβ aggregates in Caenorhabditiselegans.67 Intravitreal injection of Aβ25–35 was found to induce increased laminin in the RGCL, which was reversed by BMD treatment, contradictory to the effect of BMD treatment observed in the OHT model. Here, LAMB2 is linked to Senile plaques.