Ajinkya Limkar, MD-PhD candidate at UW–Madison and research assistant at the UW–Madison George M. O’Brien Urology Cooperative Research Center, recently published a preprint in bioRxiv journal titled, “Amyloid-beta is present in the spinal cord of APP/PS1 mice and may contribute to neuropathology manifesting as lower urinary tract dysfunction”. In this study, Ajinkya and his team investigated whether amyloid-beta plaques, a signature feature of Alzheimer’s disease (AD), may contribute to urinary incontinence (UI)

UI is a common comorbidity of AD; however, the underlying pathophysiology of UI in AD remains understudied. Using an AD mice model along with functional voiding assays, Ajinkya and his team characterized the urinary dysfunction in the mice and determined that UI was associated with bladder storage-phase abnormalities.

They then further examined the nervous system and discovered amyloid-beta deposition within both the central and peripheral nervous system of the bladder-innervation pathway, including the spinal cord, dorsal root ganglia, ventral roots, and cauda equina.

These findings suggest that UI in AD may be associated with alterations in the neurogenic pathway that may regulate bladder function, potentially contributing to urinary symptoms.

In correspondence with the CAIRIBU Interactions Core, Ajinkya credited the CAIRIBU Community with, “[bringing] together investigators with complementary interests and expertise, helping spark this collaboration and contributing significantly to its success.” He further elaborated that, “discussions at CAIRIBU interest group meetings and the annual in-person conference [inspired] new questions and helped identify additional avenues for further investigation.”