Alzheimer's disease (AD) is a neurodegenerative disease involving a variety of pathogenic factors.Studies have shown that TAR DNA-binding protein 43 (TDP-43) may cause AD pathological changes and induce cognitive dysfunction by increasing Aβ abnormal deposition,promoting Tau hyperphosphorylation,triggering mitochondrial dysfunction,and aggravating neuroinflammation.This paper reviews the important role of TDP-43 in the pathogenesis of AD.

In recent years, a large number of studies have found that Parkinson's disease (PD) patients often complicate with osteoporotic fracture, which may be related to decreased dopamine transmitters, PD risk gene mutations, mitochondrial dysfunction, vitamin D reduction, anti-PD drug use, autonomic nervous dysfunction and intestinal microflora disorders. Therefore, this paper reviews the current research progress on the pathogenesis of osteoporotic fracture in PD patients to provide theoretical basis for co-morbid treatment of PD and osteoporotic fracture.

TAR DNA/RNA-binding domain protein 43 (TDP-43) has become one of the pathogenic factors of many neurodegenerative diseases, such as Alzheimer's disease (AD). Clearance of abnormal accumulation of TDP-43 might be the potential treatment target in AD patients. Ubiquitin-proteasome system (UPS) is one of the main ways of protein clearance. UPS dysfunction plays an important role in the pathogenesis and progression of AD. This review focuses on the roles of TDP-43 and UPS in the pathogenesis of AD, as well as the research progress of UPS mediated clearance TDP-43 in the treatment of AD.