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J Neuropathol Exp Neurol. 2016 Jul;75(7):618-27. doi: 10.1093/jnen/nlw043. Epub 2016 May 31.

Protective Effects of Forskolin on Behavioral Deficits and Neuropathological Changes in a Mouse Model of Cerebral Amyloidosis.

Author information

1
From the Division of Immunopathology of the Nervous System, Institute of Pathology and Neuropathology, University of Tubingen, Tubingen, Germany (BAO, CZ, HJS, ZYZ). briceayissi03@yahoo.fr.
2
From the Division of Immunopathology of the Nervous System, Institute of Pathology and Neuropathology, University of Tubingen, Tubingen, Germany (BAO, CZ, HJS, ZYZ).

Abstract

The production of amyloid-β peptides in the brains of patients with Alzheimer disease (AD) may contribute to memory loss and impairments in social behavior. Here, an efficient adenylate cyclase activator, forskolin, was orally administered by gavage (100 mg/kg body weight) to 5-month-old transgenic APP/PS1 mice, which serve as an animal model of cerebral amyloidosis. Analyses of nest construction, sociability, and immunohistochemical features were used to determine the effects of forskolin treatment. After a relatively short term of treatment (10 days), forskolin-treated transgenic mice showed restored nest construction ability (p < 0.05) and their sociability (p < 0.01). There was a reduction of Aβ plaque deposition in the cortex and in the hippocampus. Furthermore, expression of transforming growth factor β, glial fibrillary acidic protein, and Iba-1 in the cortex was reduced in the forskolin-treated group, suggesting regulation of the inflammatory response mediated by activated microglia and astrocytes in the brains of the APP/PS1 mice (p < 0.01). Taken together, these findings suggest that forskolin shows neuroprotective effects in APP/PS1 Tg mice and may be a promising drug in the treatment of patients with AD.

KEYWORDS:

APP/PS1 transgenic mice; Alzheimer disease; Cerebral amyloidosis; Forskolin.; β-amyloid

PMID:
27251043
PMCID:
PMC4913438
DOI:
10.1093/jnen/nlw043
[Indexed for MEDLINE]
Free PMC Article

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