After the first Aβ deposits it has the ability to physically stimulate further deposition of other Aβ peptides, leading to additional reorganization and formation of neuritic plaques. According to Cummings et al., once the plaques are mature they are able to activate the neighboring tissue, including microglia and astrocytes, culminating in neuronal damage and synaptic dysfunction. This pathological scenario is thought to be a result of oxidative injury and phosphorylation linked to the presence of the plaques as well as the accumulation of the tau tangles (Lamberts et al.,
After the first Aβ deposits it has the ability to physically stimulate further deposition of other Aβ peptides, leading to additional reorganization and formation of neuritic plaques. According to Cummings et al., once the plaques are mature they are able to activate the neighboring tissue, including microglia and astrocytes, culminating in neuronal damage and synaptic dysfunction. This pathological scenario is thought to be a result of oxidative injury and phosphorylation linked to the presence of the plaques as well as the accumulation of the tau tangles (Lamberts et al.,