The effect of V-ATPase function defects in pathogenesis of Alzheimer's disease

CNS Neurosci Ther. 2018 Sep;24(9):837-840. doi: 10.1111/cns.12861. Epub 2018 May 14.

Authors

Zi-Wei Zhao¹, Zhen Yuan², De-Qiang Zhao³, Zhan-Wen Wang¹, Fei-Qi Zhu⁴, Ping Luan^{1

3}

Affiliations

¹ Medical Center, Shenzhen University Health Science Center, Shenzhen, China.
² Faculty of Health Sciences, University of Macau, Macau, China.
³ Department of Neurology, Nanfang Hospital of Southern Medical University, Guangzhou, China.
⁴ Cognitive Impairment Ward of Neurology Department, the 3rd Affiliated Hospital of Shenzhen University, Shenzhen, China.

No abstract available

Publication types

Letter
Research Support, Non-U.S. Gov't

MeSH terms

Adenosine Triphosphatases / physiology
Alzheimer Disease / genetics
Alzheimer Disease / metabolism*
Alzheimer Disease / pathology
Amyloid beta-Peptides / genetics
Amyloid beta-Peptides / metabolism*
Animals
Humans
Mice
Mice, Transgenic
Peptide Fragments / genetics
Peptide Fragments / metabolism*
Vacuolar Proton-Translocating ATPases / genetics
Vacuolar Proton-Translocating ATPases / metabolism*

Substances

Amyloid beta-Peptides
Atp6ap1 protein, mouse
Peptide Fragments
amyloid beta-protein (25-35)
Adenosine Triphosphatases
Vacuolar Proton-Translocating ATPases