Abstract
Alzheimer’s disease (AD) is characterized by the pathological accumulation of amyloid β (Aβ) plaques and neurofibrillary tangles composed of hyperphosphorylated tau. Microglia and astrocytes respond to the abnormal presence of tau protein with induced transposable element (TE) transcription. In this Forum, we discuss new data that link dysregulated TE expression to AD pathogenesis.
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