The search for a cure for AD is restless. Researchers suggest that in order to prevent or slow the progression of AD, medical interventions should be focused on treating the root cause of the disease. Normally, the brains of people with AD have an abundance of abnormal structure called amyloid plaques (sticky buildup of abnormal proteins outside nerve cells or neurons).  Recent advances in medicine have shown that brain amyloid clearance is modulated by IGF-1. [228-229] An overwhelming body of clinical research even found that patients with low IGF-1 levels in the blood are at higher risk for AD. [230-236] Interestingly, numerous studies found that higher levels of IGF-1 may help protect against degeneration of brain cells and can lower one’s risk for AD. [237-239] According to other studies assessing the therapeutic benefits of IGF-1 on brain health, the specific mechanisms by which IGF-1 may help protect against AD and other neurological disorder is that IGF-1 promotes nerve cell regeneration and prevents programmed cell death of brain cells. [240-255] These neuroprotective effects may be the reason why IGF-1 administration in patients with AD resulted in significant improvement in memory and thinking skills. 
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