Altered cerebral vascular volumes and solute transport at the blood-brain barriers of two transgenic mouse models of Alzheimer's disease

Neuropharmacology. 2014 Jun:81:311-7. doi: 10.1016/j.neuropharm.2014.02.010. Epub 2014 Mar 12.

Abstract

We evaluated the integrity and function of the blood-brain barrier in 3xTg-AD mice aged 3-18 months and in APP/PS1 mice aged 8-months to determine the impacts of changes in amyloid and tau proteins on the brain vascular changes. The vascular volume (Vvasc) was sub-normal in 3xTg-AD mice aged from 6 to 18 months, but not in the APP/PS1 mice. The uptakes of [(3)H]-diazepam by the brains of 3xTg-AD, APP/PS1 and their age-matched control mice were similar at all the times studied, suggesting that the simple diffusion of small solutes is unchanged in transgenic animals. The uptake of d-glucose by the brains of 18-month old 3xTg-AD mice, but not by those of 8-month old APP/PS1 mice, was reduced compared to their age-matched controls. Accordingly, the amount of Glut-1 protein was 1.4 times lower in the brain capillaries of 18 month-old 3xTg-AD mice than in those of age-matched control mice. We conclude that the brain vascular volume is reduced early in 3xTg-AD mice, 6 months before the appearance of pathological lesions, and that this reduction persists until they are at least 18 months old. The absence of alterations in the BBB of APP/PS1 mice suggests that hyperphosphorylated tau proteins contribute to the vascular changes that occur in AD.

Keywords: 3xTg-AD; APP/PS1; Alzheimer's disease; Blood–brain barrier integrity; Brain vascular volume; In situ brain perfusion.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Age Factors
  • Alzheimer Disease / genetics
  • Alzheimer Disease / pathology*
  • Amyloid beta-Protein Precursor / genetics
  • Animals
  • Blood-Brain Barrier / metabolism*
  • Blood-Brain Barrier / physiology*
  • Brain / drug effects
  • Brain / metabolism
  • Brain / pathology*
  • Cerebrovascular Circulation / genetics*
  • Diazepam / metabolism
  • Disease Models, Animal
  • Functional Laterality
  • Glucose / metabolism
  • Glucose Transporter Type 1 / metabolism*
  • Humans
  • Mice
  • Mice, Transgenic
  • Microvessels / pathology
  • Microvessels / physiopathology
  • Mutation / genetics
  • Presenilin-1 / genetics
  • Sucrose / metabolism
  • tau Proteins / genetics

Substances

  • Amyloid beta-Protein Precursor
  • Glucose Transporter Type 1
  • PSEN1 protein, human
  • Presenilin-1
  • Slc2a1 protein, mouse
  • tau Proteins
  • Sucrose
  • Glucose
  • Diazepam