| Abstrakt: |
A recent study conducted by researchers at the Karolinska Institute in Solna, Sweden, has shed light on the early stages of Alzheimer's disease (AD). The study focused on neurons in the entorhinal cortex (ECII) that are the first to accumulate tau protein aggregates and degenerate during prodromal AD. The researchers identified the proto-oncogene DEK as a regulator of tau pathology and found that silencing DEK led to epigenetic changes that altered activity-induced transcription and neuronal excitability. This resulted in the gradual accumulation of tau in the somatodendritic compartment of ECII neurons, microglia reactivity, and microglia-mediated neuron loss, all of which are characteristic of early AD. The study suggests that synaptic homeostasis dysregulation plays a central role in the onset of tau pathology in AD. [Extracted from the article] |
