PMID- 38218348
OWN - NLM
STAT- MEDLINE
DCOM- 20240214
LR  - 20240214
IS  - 1873-4847 (Electronic)
IS  - 0955-2863 (Linking)
VI  - 125
DP  - 2024 Mar
TI  - High salt diet exacerbates cognitive deficits and neurovascular abnormalities in 
      APP/PS1 mice and induces AD-like changes in wild-type mice.
PG  - 109570
LID - S0955-2863(24)00004-4 [pii]
LID - 10.1016/j.jnutbio.2024.109570 [doi]
AB  - High salt diet (HSD) is a risk factor of hypertension and cardiovascular disease. 
      Although clinical data do not clearly indicate the relationship between HSD and 
      the prevalence of Alzheimer's disease (AD), animal experiments have shown that 
      HSD can cause hyperphosphorylation of tau protein and cognition impairment. 
      However, whether HSD can accelerate the progression of AD by damaging the 
      function of neurovascular unit (NVU) in the brain is unclear. Here, we fed 
      APP/PS1 mice (an AD model) or wild-type mice with HSD and found that the chronic 
      HSD feeding increased the activity of enzymes related to tau phosphorylation, 
      which led to tau hyperphosphorylation in the brain. HSD also aggravated the 
      deposition of Abeta42 in hippocampus and cortex in the APP/PS1 mice but not in the 
      wild-type mice. Simultaneously, HSD caused the microglia proliferation, low 
      expression of Aqp-4, and high expression of CD31 in the wild-type mice, which 
      were accompanied with the loss of pericytes (PCs) and increase in blood brain 
      barrier (BBB) permeability. As a result, wild-type mice fed with HSD performed 
      poorly in Morris Water Maze and object recognition test. In the APP/PS1 mice, HSD 
      feeding for 8 months worsen the cognition and accompanied the loss of PCs, the 
      activation of glia, the increase in BBB permeability, and the acceleration of 
      calcification in the brain. Our data suggested that HSD feeding induced the 
      AD-like pathology in wild-type mice and aggravated the development of AD-like 
      pathology in APP/PS1 mice, which implicated the tau hyperphosphorylation and NVU 
      dysfunction.
CI  - Copyright (c) 2024. Published by Elsevier Inc.
FAU - Chen, Hai Chao
AU  - Chen HC
AD  - Institute of Anatomy and Histology & Embryology, Neuroscience, School of Basic 
      Medical Sciences, Lanzhou University, Lanzhou, Gansu, People's Republic of China.
FAU - Cao, Jia-Xin
AU  - Cao JX
AD  - Institute of Anatomy and Histology & Embryology, Neuroscience, School of Basic 
      Medical Sciences, Lanzhou University, Lanzhou, Gansu, People's Republic of China.
FAU - Zhang, Yi-Shu
AU  - Zhang YS
AD  - Institute of Anatomy and Histology & Embryology, Neuroscience, School of Basic 
      Medical Sciences, Lanzhou University, Lanzhou, Gansu, People's Republic of China.
FAU - Ma, Yue-Zhang
AU  - Ma YZ
AD  - Institute of Biochemistry and Molecular Biology, School of Basic Medical 
      Sciences, Lanzhou University, Lanzhou, Gansu, People's Republic of China.
FAU - Zhang, Lu
AU  - Zhang L
AD  - Institute of Anatomy and Histology & Embryology, Neuroscience, School of Basic 
      Medical Sciences, Lanzhou University, Lanzhou, Gansu, People's Republic of China.
FAU - Su, Xiao-Mei
AU  - Su XM
AD  - Institute of Anatomy and Histology & Embryology, Neuroscience, School of Basic 
      Medical Sciences, Lanzhou University, Lanzhou, Gansu, People's Republic of China.
FAU - Gao, Li-Ping
AU  - Gao LP
AD  - Institute of Biochemistry and Molecular Biology, School of Basic Medical 
      Sciences, Lanzhou University, Lanzhou, Gansu, People's Republic of China.
FAU - Jing, Yu-Hong
AU  - Jing YH
AD  - Institute of Anatomy and Histology & Embryology, Neuroscience, School of Basic 
      Medical Sciences, Lanzhou University, Lanzhou, Gansu, People's Republic of China; 
      Key Laboratory of Preclinical Study for New Drugs of Gansu province, Lanzhou 
      University, Lanzhou, Gansu, People's Republic of China. Electronic address: 
      jingyh@lzu.edu.cn.
LA  - eng
PT  - Journal Article
DEP - 20240111
PL  - United States
TA  - J Nutr Biochem
JT  - The Journal of nutritional biochemistry
JID - 9010081
RN  - 0 (Amyloid beta-Peptides)
RN  - 0 (tau Proteins)
RN  - 0 (Sodium Chloride, Dietary)
RN  - 0 (Amyloid beta-Protein Precursor)
RN  - 0 (Presenilin-1)
SB  - IM
MH  - Mice
MH  - Animals
MH  - *Alzheimer Disease/metabolism
MH  - Amyloid beta-Peptides/metabolism
MH  - Mice, Transgenic
MH  - tau Proteins/metabolism
MH  - Diet
MH  - Cognition
MH  - Sodium Chloride, Dietary/adverse effects
MH  - Disease Models, Animal
MH  - Amyloid beta-Protein Precursor/genetics/metabolism
MH  - Presenilin-1/genetics/metabolism
OTO - NOTNLM
OT  - Abeta
OT  - Blood-brain barrier
OT  - High salt diet
OT  - Neurovascular unit
OT  - p-Tau
COIS- Declaration of interest The authors declare that they have no competing 
      interests.
EDAT- 2024/01/14 12:42
MHDA- 2024/02/12 05:43
CRDT- 2024/01/13 19:30
PHST- 2023/06/13 00:00 [received]
PHST- 2023/12/25 00:00 [revised]
PHST- 2024/01/03 00:00 [accepted]
PHST- 2024/02/12 05:43 [medline]
PHST- 2024/01/14 12:42 [pubmed]
PHST- 2024/01/13 19:30 [entrez]
AID - S0955-2863(24)00004-4 [pii]
AID - 10.1016/j.jnutbio.2024.109570 [doi]
PST - ppublish
SO  - J Nutr Biochem. 2024 Mar;125:109570. doi: 10.1016/j.jnutbio.2024.109570. Epub 
      2024 Jan 11.