Oral administration of thioflavin t prevents beta amyloid plaque formation in double transgenic ad mice

Sumit Sarkar, James Raymick, Balmiki Ray, Debomoy Lahiri, Merle G. Paule, Larry Schmued

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder and the fourth leading cause of death in the United States and most common cause of adult-onset dementia. The major hallmarks of AD are the formation of senile amyloid plaques made of beta amyloid and neurofibrillary tangles (NFT) which are primarily composed of phosphorylated tau protein. Although numerous agents have been considered as providing protection against AD, identification of potential agents with neuroprotective ability is limited. Thioflavin T has been used in the past to stain amyloid beta plaques in brain. In this study, Thioflavin T (ThT) and vehicle (infant formula) were administered orally by gavage to transgenic (B6C3 APP PS1; AD-Tg) mice beginning at 4 months age and continuing until sacrifice at 9 months of age at 40mg/kg dose. The number of amyloid plaques was reduced dramatically by ThT treatment in both male and female transgenic mice compared to those in control mice. Additionally, GFAP and Amylo-Glo labeling suggest that astrocytic hypertrophy is minimized in ThT-treated animals. Similarly, CD68 labeling, which detects activated microglia, along with Amylo-Glo labeling, suggests that microglial activation is significantly less in ThT-treated mice. Both Aβ-40 and Aβ-42 concentrations in blood rose significantly in the ThT-treated animals suggesting that ThT may inhibit the deposition, degradation, and/or clearance of Aβ plaques in brain.

Original languageEnglish (US)
Pages (from-to)837-846
Number of pages10
JournalCurrent Alzheimer Research
Volume12
Issue number9
StatePublished - Nov 1 2015

Fingerprint

Amyloid Plaques
Transgenic Mice
Oral Administration
Alzheimer Disease
tau Proteins
Neurofibrillary Tangles
Infant Formula
Aptitude
Brain
Microglia
Neuroprotective Agents
thioflavin T
Amyloid
Neurodegenerative Diseases
Hypertrophy
Dementia
Cause of Death
Coloring Agents

Keywords

  • AD
  • Amylo-Glo
  • Astrocytes
  • CD68
  • GFAP
  • Microglia
  • Neuroprotection
  • Thioflavin T

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

Cite this

Oral administration of thioflavin t prevents beta amyloid plaque formation in double transgenic ad mice. / Sarkar, Sumit; Raymick, James; Ray, Balmiki; Lahiri, Debomoy; Paule, Merle G.; Schmued, Larry.

In: Current Alzheimer Research, Vol. 12, No. 9, 01.11.2015, p. 837-846.

Research output: Contribution to journalArticle

Sarkar, S, Raymick, J, Ray, B, Lahiri, D, Paule, MG & Schmued, L 2015, 'Oral administration of thioflavin t prevents beta amyloid plaque formation in double transgenic ad mice', Current Alzheimer Research, vol. 12, no. 9, pp. 837-846.
Sarkar, Sumit ; Raymick, James ; Ray, Balmiki ; Lahiri, Debomoy ; Paule, Merle G. ; Schmued, Larry. / Oral administration of thioflavin t prevents beta amyloid plaque formation in double transgenic ad mice. In: Current Alzheimer Research. 2015 ; Vol. 12, No. 9. pp. 837-846.
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