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The development of many neurodegenerative diseases is assumed to be determined by the pattern-fixed misfolding, seeded accumulation and cell–cell transmission of characteristic disease-related proteins, leading to the sequential diffusion of pathological protein aggregates. Recent indication strongly proposes that the functional connections made by neurons-in addition to the inherent physiognomies of neurons, such as morphology and gene expression profile-determine whether they are vulnerable to degeneration in these disorders. Notably, this common pathogenic principle opens up opportunities for pursuing novel targets for therapeutic interventions for these neurodegenerative disorders. We review recent evidence that supports the notion of neuron–neuron protein propagation, with a focus on neuropathological and positron emission tomography imaging studies in humans.
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