Cox TO, Devason AS, de Araujo A, Mason S, Subramanian M, Salvador AFM, Descamps HC, Kim J, Zhu Y, Litichevskiy L, Jung S, Song WS, Cortés-Martín A, Henderson NT, Huang KP, Nguyen T, Sae-Lee W, Umana IC, Sacta M, Rahman RJ, Wisser S, Nelson JAD, Golynker I, McSween AM, Hohmann EF, Patel S, Bub AL, Soekler C, Blank N, Hoxha K, Boccia L, Wong AC, Bahnsen K, Kim J, Biderman N, Abbasian D, Shoffler C, Petucci C, McAllister FE, Alhadeff AL, Fuccillo MV, Hill C, Jang C, Betley JN, de Lartigue G, Lee VY, Levy M, Thaiss CA (2026) Intestinal interoceptive dysfunction drives age-associated cognitive decline. Nature 652(8109):442-450. doi: 10.1038/s41586-026-10191-6 PMID: 41813891
Objective: To identify a mechanism by which inhibition of gut–brain signalling during ageing results in impaired neuronal activation in the hippocampus and loss of memory encoding.
Summary: The gastrointestinal microbiome has recently emerged as an important factor in the regulation of cognition and has been implicated as a modifiable peripheral signal that may contribute to age-associated memory loss. However, the circuits by which gut microbial signals are transmitted to the brain to modulate memory remain largely unclear. The authors evaluated CCKAR+ neurons to determine their role in cognitive decline.
Usage: CCK–SAP (IT-31) or Blank-SAP (IT-21) was injected (125 ng in 0.5 μl per ganglion).
Related Products: CCK-SAP (Cat. #IT-31), Blank-SAP (Cat. #IT-21)