Protein aggregation is a pathological hallmark of and may play a central role in 
the neurotoxicity in age-associated neurodegenerative diseases, such as 
Alzheimer's disease and Parkinson's disease. Accordingly, inhibiting aggregation 
of amyloidogenic proteins, including amyloid β and α-synuclein, has been a main 
therapeutic target for these disorders. Among various strategies, amyloid β 
immunotherapy has been extensively investigated in Alzheimer's disease, followed 
by similar studies of α-synuclein in Parkinson's disease. Notably, a recent 
study of solanezumab, an amyloid β monoclonal antibody, raises hope for the 
further therapeutic potential of immunotherapy, not only in Alzheimer's disease, 
but also for other neurodegenerative disorders, including Parkinson's disease. 
Thus, it is expected that further refinement of immunotherapy against 
neurodegenerative diseases may lead to increasing efficacy. Meanwhile, type II 
diabetes mellitus has been associated with an increased risk of 
neurodegenerative disease, such as Alzheimer's disease and Parkinson's disease, 
and studies have shown that metabolic dysfunction and abnormalities surrounding 
insulin signaling may underlie disease progression. Naturally, "anti-insulin 
resistance" therapy has emerged as a novel paradigm in the therapy of 
neurodegenerative diseases. Indeed, incretin agonists, which stimulate 
pancreatic insulin secretion, reduce dopaminergic neuronal loss and suppress 
Parkinson's disease disease progression in clinical trials. Similar studies are 
ongoing also in Alzheimer's disease. This paper focuses on critical issues in 
"immunotherapy" and "anti-insulin resistance" therapy in relation to therapeutic 
strategies against neurodegenerative disease, and more importantly, how they 
might merge mechanistically at the point of suppression of protein aggregation, 
raising the possibility that combined immunotherapy and "anti-insulin 
resistance" therapy may be superior to either monotherapy.