β-amyloid deposition is shifted to the vasculature and memory impairment is exacerbated when hyperhomocysteinemia is induced in APP/PS1 transgenic mice

Documenti analoghi

• Transition from an M1 to a mixed neuroinflammatory phenotype increases amyloid deposition in APP/PS1 transgenic mice
  di: Weekman, Erica M, et al.
  Pubblicazione: (2014)
• Determining the role of IL-4 induced neuroinflammation in microglial activity and amyloid-β using BV2 microglial cells and APP/PS1 transgenic mice
  di: Latta, Clare H, et al.
  Pubblicazione: (2015)
• Therapeutic Trem2 activation ameliorates amyloid-beta deposition and improves cognition in the 5XFAD model of amyloid deposition
  di: Price, Brittani R., et al.
  Pubblicazione: (2020)
• Hyperhomocysteinemia-Induced Gene Expression Changes in the Cell Types of the Brain
  di: Weekman, Erica M., et al.
  Pubblicazione: (2017)
• Time course of neuropathological events in hyperhomocysteinemic amyloid depositing mice reveals early neuroinflammatory changes that precede amyloid changes and cerebrovascular events
  di: Weekman, Erica M., et al.
  Pubblicazione: (2019)