Alzheimer's disease (AD) is characterized by the coexistence of amyloid-β (Aβ) plaques and tau-based neurofibrillary tangles. Although studies have shown that the interaction between Aβ and tau causes enhanced AD pathology; there is a lack of precise understanding of the functional consequences for integrated neural circuits. A recent study revealed that the interaction between Aβ and tau pathologies impairs the functional integrity of neural circuits in the AD brain. Thus, not only Aβ but also tau determines the cognitive status. Therefore, developing anti-Aβ or anti-aggregated tau compounds may not be an effective strategy to treat AD. In fact, approaches combining anti-Aβ and anti-tau therapies might be a more promising therapeutic option rather than single therapy. The results have important therapeutic implications not only for AD but also for other tauopathies.
Keywords: Aggregation; neural hyperactivity; neural silencing; neurofibrillary tangles; plaques; transgenic mice.