Yingshuai Li
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Yingshuai Li has a total of 5 co-authors. Here are the top co-authors by number of shared publications:
- Dongjun Jiang
Shandong Collaborative Innovation Center for Diagnosis, Treatment and Behavioral Interventions of Mental Disorders, Institute of Mental Health, Jining Medical University, Jining 272067, China
1 shared publication - Fengjuan Jiao
Shandong Collaborative Innovation Center for Diagnosis, Treatment and Behavioral Interventions of Mental Disorders, Institute of Mental Health, Jining Medical University, Jianshe South Road No.45, Rencheng District, Jining 272013, China
1 shared publication - Juan Mei
Shandong Collaborative Innovation Center for Diagnosis, Treatment and Behavioral Interventions of Mental Disorders, Institute of Mental Health, Jining Medical University, Jianshe South Road No.45, Rencheng District, Jining 272013, China
1 shared publication - Qinqin Wang
School of Mental Health, Jining Medical University, Jining, China
1 shared publication - Xue-Zhi Li
School of Mathematics and Statistics, Henan Normal University, Xinxiang, China
1 shared publication
Latest Publications
- Open Access
Amyloidogenesis and Neurotrophic Dysfunction in Alzheimer’s Disease: Do They have a Common Regulating Pathway?
The amyloid cascade hypothesis has predominately been used to describe the pathogenesis of Alzheimer’s disease (AD) for decades, as Aβ oligomers are thought to be the prime cause of AD. Meanwhile, the neurotrophic factor hypothesis has also been proposed for decades. Accumulating evidence states that the amyloidogenic process and neurotrophic dysfunction are mutually influenced and may coincidently cause the onset and progress of AD. Meanwhile, there are intracellular regulators participating both in the amyloidogenic process and neurotrophic pathways, which might be the common original causes of amyloidogenesis and neurotrophic dysfunction. In this review, the current understanding regarding the role of neurotrophic dysfunction and the amyloidogenic process in AD pathology is briefly summarized. The mutual influence of these two pathogenesis pathways and their potential common causal pathway are further discussed. Therapeutic strategies targeting the common pathways to simultaneously prevent amyloidogenesis and neurotrophic dysfunction might be anticipated for the disease-modifying treatment of AD.
Open AccessAmyloidogenesis and Neurotrophic Dysfunction in Alzheimer’s Disease: Do They have a Common Regulating Pathway?
The amyloid cascade hypothesis has predominately been used to describe the pathogenesis of Alzheimer’s disease (AD) for decades, as Aβ oligomers are thought to be the prime cause of AD. Meanwhile, the neurotrophic factor hypothesis has also been proposed for decades. Accumulating evidence states that the amyloidogenic process and neurotrophic dysfunction are mutually influenced and may coincidently cause the onset and progress of AD. Meanwhile, there are intracellular regulators participating both in the amyloidogenic process and neurotrophic pathways, which might be the common original causes of amyloidogenesis and neurotrophic dysfunction. In this review, the current understanding regarding the role of neurotrophic dysfunction and the amyloidogenic process in AD pathology is briefly summarized. The mutual influence of these two pathogenesis pathways and their potential common causal pathway are further discussed. Therapeutic strategies targeting the common pathways to simultaneously prevent amyloidogenesis and neurotrophic dysfunction might be anticipated for the disease-modifying treatment of AD.