Paper s10522-024-10181-z.pdf

Alzheimer's disease (AD) and osteoporosis (OP) pose distinct but  interconnected health challenges, both significantly impacting the aging  population. AD, a neurodegenerative disorder characterized by memory  impairment and cognitive decline, is primarily associated with the  accumulation of abnormally folded amyloid beta (Aβ) peptides and  neurofibrillary tangles in the brain. OP, a skeletal disorder marked by  low bone mineral density, involves dysregulation of bone remodeling and  is associated with an increased risk of fractures. Recent studies have  revealed an intriguing link between AD and OP, highlighting shared  pathological features indicative of common regulatory pathophysiological  pathways. In this article, we elucidate the signaling mechanisms that  regulate the pathology of AD and OP and offer insights into the  intricate network of factors contributing to these conditions. We also  examine the role of bone-derived factors in the progression of AD,  underscoring the plausibility of bidirectional communication between the  brain and the skeletal system. The presence of amyloid plaques in the  brain of individuals with AD is akin to the accumulation of brain Aβ in  vascular dementia, pointing towards the need for further investigation  of shared molecular mechanisms. Moreover, we discuss the role of  bone-derived microRNAs that may regulate the pathological progression of  AD, providing a novel perspective on the role of skeletal factors in  neurodegenerative diseases. The insights presented here should help  researchers engaged in exploring innovative therapeutic approaches  targeting both neurodegenerative and skeletal disorders in aging  populations.