PMID- 34018152
OWN - NLM
STAT- MEDLINE
DCOM- 20220207
LR  - 20220207
IS  - 1559-1182 (Electronic)
IS  - 0893-7648 (Linking)
VI  - 58
IP  - 9
DP  - 2021 Sep
TI  - Disruption of Circadian Clocks Promotes Progression of Alzheimer's Disease in 
      Diabetic Mice.
PG  - 4404-4412
LID - 10.1007/s12035-021-02425-7 [doi]
AB  - The circadian clock is an endogenous system designed to anticipate and adapt to 
      daily changes in the environment. Alzheimer's disease (AD) is a progressive 
      neurodegenerative disease, which is more prevalent in patients with type 2 
      diabetes mellitus (T2DM). However, the effects of circadian disruption on mental 
      and physical health for T2DM patients are not yet fully understood, even though 
      circadian disruption has been confirmed to promote the progression of AD in 
      population. By housing db/db mice on a disrupted (a 6:18 light/dark cycle) 
      circadian rhythm, we assessed the circadian gene expression, body weight, 
      cognitive ability, and AD-related pathophysiology. Our results indicated that 
      housing in these conditions led to disrupted diurnal circadian rhythms in the 
      hippocampus of db/db mice and contributed to their weight gain. In the brain, the 
      circadian-disrupted db/db mice showed a decreased cognitive ability and an 
      increased hyperphosphorylation of tau protein, even though no difference was 
      found in amyloid protein (Abeta) plaque deposition. We also found that the 
      hyperphosphorylated tau protein exhibited more disruptive daily oscillations in 
      db/db mice hippocampus under the 6:18 light/dark cycle. Circadian alterations 
      could promote the development of AD in T2DM.
CI  - (c) 2021. The Author(s), under exclusive licence to Springer Science+Business 
      Media, LLC, part of Springer Nature.
FAU - Huang, Jiaojiao
AU  - Huang J
AD  - Department of Endocrinology, Tongji Hospital, Tongji Medical College, Huazhong 
      University of Science and Technology, Wuhan, 430030, Hubei, China.
FAU - Peng, Xuemin
AU  - Peng X
AD  - Department of Endocrinology, Tongji Hospital, Tongji Medical College, Huazhong 
      University of Science and Technology, Wuhan, 430030, Hubei, China.
FAU - Fan, Rongping
AU  - Fan R
AD  - Department of Endocrinology, Tongji Hospital, Tongji Medical College, Huazhong 
      University of Science and Technology, Wuhan, 430030, Hubei, China.
FAU - Dong, Kun
AU  - Dong K
AD  - Department of Endocrinology, Tongji Hospital, Tongji Medical College, Huazhong 
      University of Science and Technology, Wuhan, 430030, Hubei, China.
AD  - Branch of National Clinical Research Center for Metabolic Diseases, Wuhan, Hubei, 
      China.
FAU - Shi, Xiaoli
AU  - Shi X
AD  - Department of Endocrinology, Tongji Hospital, Tongji Medical College, Huazhong 
      University of Science and Technology, Wuhan, 430030, Hubei, China.
AD  - Branch of National Clinical Research Center for Metabolic Diseases, Wuhan, Hubei, 
      China.
FAU - Zhang, Shujun
AU  - Zhang S
AD  - Department of Endocrinology, Tongji Hospital, Tongji Medical College, Huazhong 
      University of Science and Technology, Wuhan, 430030, Hubei, China.
AD  - Branch of National Clinical Research Center for Metabolic Diseases, Wuhan, Hubei, 
      China.
FAU - Yu, Xuefeng
AU  - Yu X
AD  - Department of Endocrinology, Tongji Hospital, Tongji Medical College, Huazhong 
      University of Science and Technology, Wuhan, 430030, Hubei, China.
AD  - Branch of National Clinical Research Center for Metabolic Diseases, Wuhan, Hubei, 
      China.
FAU - Yang, Yan
AU  - Yang Y
AUID- ORCID: 0000-0001-8146-8040
AD  - Department of Endocrinology, Tongji Hospital, Tongji Medical College, Huazhong 
      University of Science and Technology, Wuhan, 430030, Hubei, China. 
      yangyan6910@163.com.
AD  - Branch of National Clinical Research Center for Metabolic Diseases, Wuhan, Hubei, 
      China. yangyan6910@163.com.
LA  - eng
GR  - 81670754/National Natural Science Foundation of China/
GR  - 81974114/National Natural Science Foundation of China/
GR  - 81800686/National Natural Science Foundation of China/
GR  - 2018076/Jie Chu Jing Ying foundation/
PT  - Journal Article
DEP - 20210521
PL  - United States
TA  - Mol Neurobiol
JT  - Molecular neurobiology
JID - 8900963
SB  - IM
MH  - Alzheimer Disease/*physiopathology
MH  - Animals
MH  - Behavior, Animal/physiology
MH  - Circadian Clocks/*physiology
MH  - Diabetes Mellitus, Type 2/*physiopathology
MH  - Disease Models, Animal
MH  - Disease Progression
MH  - Maze Learning/*physiology
MH  - Mice
MH  - Motor Activity/physiology
MH  - Photoperiod
MH  - Recognition, Psychology/*physiology
OTO - NOTNLM
OT  - Alzheimer's disease
OT  - Circadian rhythms
OT  - Light
OT  - Type 2 diabetes mellitus
EDAT- 2021/05/22 06:00
MHDA- 2022/02/08 06:00
CRDT- 2021/05/21 06:43
PHST- 2021/02/16 00:00 [received]
PHST- 2021/05/07 00:00 [accepted]
PHST- 2021/05/22 06:00 [pubmed]
PHST- 2022/02/08 06:00 [medline]
PHST- 2021/05/21 06:43 [entrez]
AID - 10.1007/s12035-021-02425-7 [pii]
AID - 10.1007/s12035-021-02425-7 [doi]
PST - ppublish
SO  - Mol Neurobiol. 2021 Sep;58(9):4404-4412. doi: 10.1007/s12035-021-02425-7. Epub 
      2021 May 21.