A large and growing body of literature implicates ADDLs as the molecular cause of AD:

• When applied to sections of brain tissue, ADDLs attack hippocampal CA1 nerve cells but not CA3 or cerebellar nerve cells, exactly replicating the unique pattern of damage in AD brain.  By contrast, fibrillar amyloid damages nerve cells in all brain regions and cannot explain AD pathology.
• When ADDLs are injected directly into animal brains, learning and memory functions fail and the underlying Long Term Potentiation process is blocked.
• ADDLs attack nerve cells directly by binding tightly to receptor proteins at synapses, which triggers abnormal signaling and interferes with neuronal biochemistry essential to learning.
• ADDL signaling triggers phosphorylation of the tau protein, leading to formation of tangles. By this process, ADDLs unify the two predominant, but conflicting hypotheses routinely invoke to explain AD.
• ADDLs are present at >70 fold concentrations in AD brain tissue compared unaffected, age-matched tissue.
• Transgenic animals engineered to generate excess of Abeta 42 exhibit memory deficits that increase in severity as ADDL levels increase.



• Treatment of these transgenic animals with prototype anti-ADDL therapeutics reverses memory deficits and restores learning ability.