Topic: Tau aggregates

Spontaneous neuronal activity (SNA) plays an important role in the maturation and refinement of neuronal connections. However, neurodegenerative diseases, like tauopathies, can significantly alter SNA. Changes in SNA after the expression of tau mutations have not yet been analysed at presymptomatic stages. Furthermore, the currently available models lack the necessary complexity of the human brain to fully understand the underlying mechanisms of tau pathology and its effects on SNA. To address this, we present a novel in vitro platform utilizing cortical organoids (COs), derived from hPSCs, to

Mouse models are valuable tools for investigating pathogenic mechanisms related to neurodegeneration. For Alzheimer's disease, several animal models have been generated which recapitulate critical aspects of the disease, such as accumulation of Tau aggregates accompanied by neuronal loss and brain atrophy. However, the detailed mechanisms of how these events occur are still not fully understood. To determine the temporal relationship between Tau pathology and neuronal loss, we used JNPL3 transgenic mice, which express human Tau with P301L mutation. JNPL3 mice develop Tau neurofibrillary tangle