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Although more PD models are needed to validate whether PKM2 is a universal therapeutic target in PD, our results provide preliminary evidence that dimerizing PKM2 is a potential therapeutic approach to protect nigral dopaminergic neurons from oxidative damage

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As mentioned, the binding sites of amylin are similar to calcitonin binding sites due to the discussed structural resemblance of their receptors

Evaluation of cell-specific alterations in alzheimers disease and relevance of in vitro models