AI Article Synopsis
- Alzheimer's disease (AD) not only affects cognitive functions but also leads to changes in bone metabolism, resulting in lower bone density and strength in affected individuals.
- Recent research on AD mice showed that targeting specific autophagy receptors, Optineurin (OPTN) and Sequestosome 1 (SQSTM1), improved bone health and reduced amyloid beta (Aβ) deposits in bone tissue.
- This study highlights the potential of targeting autophagy as a dual therapeutic strategy to address both AD and osteoporosis, suggesting that Aβ deposition may link the two conditions.
Article Abstract
Alzheimer's disease (AD) is a common degenerative disease among the elderly population. In addition to cognitive impairment, AD is often accompanied by behavioral manifestations. However, little attention has been paid to changes in bone metabolism and related mechanisms in patients with AD. We found that AD mice (APPswe/PS1dE9) had reduced bone density, weakened bone strength, and amyloid beta (Aβ) deposition in the bone tissue. It was further found that targeting autophagy receptors Optineurin (OPTN) and Sequestosome 1 (SQSTM1) increased bone density and bone strength in AD mice, promoted the clearance of Aβ in the bone tissue, and maintained bone homeostasis. Our study suggests that abnormal Aβ deposition may be the co-pathogenesis of AD and osteoporosis (OP). Targeting OPTN and SQSTM1 has a dual-functional effect of alleviating both AD and OP through selective autophagy that specifically targets Aβ for clearance. Therapeutic strategies targeting autophagy may help guide the treatment of patients with AD complicated with OP.
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| http://dx.doi.org/10.1016/j.cbi.2023.110462 | DOI Listing |
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