PMID- 25471187
OWN - NLM
STAT- MEDLINE
DCOM- 20160229
LR  - 20150304
IS  - 1875-8908 (Electronic)
IS  - 1387-2877 (Linking)
VI  - 45
IP  - 1
DP  - 2015
TI  - Type 2 diabetes aggravates Alzheimer's disease-associated vascular alterations of 
      the aorta in mice.
PG  - 127-38
LID - 10.3233/JAD-141008 [doi]
AB  - Vascular risk factors are associated with a higher incidence of dementia. In 
      fact, diabetes mellitus is considered a main risk factor for Alzheimer's disease 
      (AD) and both diseases are characterized by vascular dysfunction. However, the 
      underlying mechanisms remain largely unknown. Here, the effects of 
      high-sucrose-induced type 2 diabetes (T2D) in the aorta of wild type (WT) and 
      triple-transgenic AD (3xTg-AD) mice were investigated. 3xTg-AD mice showed a 
      significant decrease in body weight and an increase in postprandial glycemia, 
      glycated hemoglobin (HbA1c), and vascular nitrotyrosine, superoxide anion (O2*-), 
      receptor for the advanced glycation end products (RAGE) protein, and monocyte 
      chemoattractant protein-1 (MCP-1) levels when compared to WT mice. High-sucrose 
      intake caused a significant increase in body weight, postprandial glycemia, 
      HbA1c, triglycerides, plasma vascular cell adhesion molecule 1 (VCAM-1), and 
      vascular nitrotyrosine, O2*-, RAGE, and MCP-1 levels in both WT and 3xTg-AD mice 
      when compared to the respective control group. Also, a significant decrease in 
      nitric oxide-dependent vasorelaxation was observed in 3xTg-AD and sucrose-treated 
      WT mice. In conclusion, AD and T2D promote similar vascular dysfunction of the 
      aorta, this effect being associated with elevated oxidative and nitrosative 
      stress and inflammation. Also, AD-associated vascular alterations are potentiated 
      by T2D. These findings support the idea that metabolic alterations predispose to 
      the onset and progression of dementia.
FAU - Sena, Cristina M
AU  - Sena CM
AD  - Institute of Physiology, Faculty of Medicine, University of Coimbra, Coimbra, 
      Portgual IBILI - Institute of Biomedical Imaging and Life Sciences, Faculty of 
      Medicine, University of Coimbra, Coimbra, Portugal.
FAU - Pereira, Ana M
AU  - Pereira AM
AD  - Institute of Physiology, Faculty of Medicine, University of Coimbra, Coimbra, 
      Portgual IBILI - Institute of Biomedical Imaging and Life Sciences, Faculty of 
      Medicine, University of Coimbra, Coimbra, Portugal.
FAU - Carvalho, Cristina
AU  - Carvalho C
AD  - CNC - Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, 
      Portugal.
FAU - Fernandes, Rosa
AU  - Fernandes R
AD  - IBILI - Institute of Biomedical Imaging and Life Sciences, Faculty of Medicine, 
      University of Coimbra, Coimbra, Portugal.
FAU - Seica, Raquel M
AU  - Seica RM
AD  - Institute of Physiology, Faculty of Medicine, University of Coimbra, Coimbra, 
      Portgual IBILI - Institute of Biomedical Imaging and Life Sciences, Faculty of 
      Medicine, University of Coimbra, Coimbra, Portugal.
FAU - Oliveira, Catarina R
AU  - Oliveira CR
AD  - Institute of Biochemistry, Faculty of Medicine, University of Coimbra, Coimbra, 
      Portugal CNC - Center for Neuroscience and Cell Biology, University of Coimbra, 
      Coimbra, Portugal.
FAU - Moreira, Paula I
AU  - Moreira PI
AD  - Institute of Physiology, Faculty of Medicine, University of Coimbra, Coimbra, 
      Portgual CNC - Center for Neuroscience and Cell Biology, University of Coimbra, 
      Coimbra, Portugal.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - J Alzheimers Dis
JT  - Journal of Alzheimer's disease : JAD
JID - 9814863
RN  - 0 (Amyloid beta-Protein Precursor)
RN  - 0 (Endothelin-1)
RN  - 0 (PSEN1 protein, human)
RN  - 0 (Presenilin-1)
RN  - 0 (Vasodilator Agents)
RN  - 0 (tau Proteins)
RN  - 169D1260KM (Nitroprusside)
RN  - EC 1.15.1.1 (Superoxide Dismutase)
RN  - N9YNS0M02X (Acetylcholine)
SB  - IM
MH  - Acetylcholine/metabolism/pharmacology
MH  - Alzheimer Disease/*complications/genetics/*pathology
MH  - Amyloid beta-Protein Precursor/genetics
MH  - Analysis of Variance
MH  - Animals
MH  - Aorta/drug effects/metabolism/*pathology
MH  - Diabetes Mellitus, Type 2/*complications
MH  - Disease Models, Animal
MH  - Endothelin-1/metabolism
MH  - Humans
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Transgenic
MH  - Mutation/genetics
MH  - Nitroprusside/pharmacology
MH  - Presenilin-1/genetics
MH  - Superoxide Dismutase/metabolism
MH  - Vasodilator Agents/pharmacology
MH  - tau Proteins/genetics
OTO - NOTNLM
OT  - Alzheimer's disease
OT  - aorta
OT  - endothelium
OT  - inflammation
OT  - oxidative stress
OT  - type 2 diabetes
EDAT- 2014/12/05 06:00
MHDA- 2016/03/02 06:00
CRDT- 2014/12/05 06:00
PHST- 2014/12/05 06:00 [entrez]
PHST- 2014/12/05 06:00 [pubmed]
PHST- 2016/03/02 06:00 [medline]
AID - A31257045V545M6X [pii]
AID - 10.3233/JAD-141008 [doi]
PST - ppublish
SO  - J Alzheimers Dis. 2015;45(1):127-38. doi: 10.3233/JAD-141008.