Dystonin/BPAG1 modulates diabetes and Alzheimer's disease cross-talk: a meta-analysis.
Jack ChengHsin-Ping LiuSu-Lun HwangLee-Fen HsuWei-Yong LinFuu-Jen TsaiPublished in: Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology (2019)
Dementia is one of the diabetic complications under intensive study. Alteration of synaptic adhesion protein (SAP) associates with neurological diseases, including Alzheimer's disease. However, the regulation of SAPs in the brain of diabetes mellitus remains elusive. To pinpoint the candidate SAPs underlining the mechanism of diabetic dementia, we investigated expression profiling of SAPs in both streptozotocin (STZ)-induced diabetic mice, AppNL-G-F/NL-G-F mice, and amyloid precursor protein intracellular domain (AICD)-induced human neural cell line from public databases. DST (Dystonin/BPAG1) was identified upregulated in both models. Our finding suggests that DST alteration may involve in the mechanism of diabetic dementia.
Keyphrases
- diabetic rats
- mild cognitive impairment
- type diabetes
- cognitive decline
- oxidative stress
- cognitive impairment
- high glucose
- wound healing
- endothelial cells
- glycemic control
- cardiovascular disease
- drug induced
- binding protein
- genome wide
- amino acid
- adipose tissue
- escherichia coli
- high resolution
- mass spectrometry
- small molecule
- metabolic syndrome
- transcription factor
- big data
- high fat diet induced
- risk factors
- subarachnoid hemorrhage
- atomic force microscopy
- blood brain barrier
- adverse drug
- single molecule
- candida albicans