Alzheimer's research uncovers sleep‑linked microglia role and experimental antisense drug slows disease

Researchers at the University of Kentaki discovered that overactive microglia—immune cells in the brain—disrupt deep NREM sleep in mouse models of Alzheimer’s disease. By limiting microglial activity, the mice recovered more than two hours of restorative sleep each day, indicating that immune‑brain interactions may be a therapeutic target.

At the recent International Alzheimer’s Association conference, Biogen presented trial data on its antisense oligonucleotide drug dinranesine, which targets the tau protein. In a study of 400 early‑stage patients, the treatment lowered cerebrospinal‑fluid tau by 50‑70% over 18 months and reduced the primary cognitive‑decline measure by 26%. An unexpected result showed the smallest dose produced the greatest improvement, underscoring the potential of tau‑targeting therapies and suggesting that combining them with anti‑amyloid approaches could yield stronger effects.