当前位置： SCI文献检索 > PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY期刊下所有文献 > Interferon beta ameliorates cognitive dysfunction in a rat model of Alzheimer's disease: Modulation of hippocampal neurogenesis and apoptosis as underlying mechanism.

Interferon beta ameliorates cognitive dysfunction in a rat model of Alzheimer's disease: Modulation of hippocampal neurogenesis and apoptosis as underlying mechanism.

Abstract：

:Neuronal apoptosis and impaired hippocampal neurogenesis are major players in cognitive/memory dysfunctions including Alzheimer's disease (AD). Interferon beta (IFNβ) is a cytokine with anti-apoptotic and neuroprotective properties on the central nervous system (CNS) cells which specifically affects neural progenitor cells (NPCs) even in the adult brain. In this study, we examined the effect of IFNβ on memory impairment as well as hippocampal neurogenesis and apoptosis in a rat model of AD. AD model was induced by lentiviral-mediated overexpression of mutant APP in the hippocampus of adult rats. Intranasal (IN) administration of IFNβ (0.5 μg/kg and 1 μg/kg doses) was started from day 23 after virus injection and continued every other day to the final day of experiments. The expression levels of APP, neurogenesis (Nestin, Ki67, DCX, and Reelin) and apoptosis (Bax/Bcl-2 ratio, cleaved-caspase-3 and seladin-1) markers were evaluated by immunohistochemistry, real-time PCR, immunofluorescence and western blotting. Moreover, thioflavin T and Nissl stainings were used to assess Aβ plaque levels and neuronal degeneration in the hippocampus, respectively. Our results showed that IFNβ treatment reduced APP expression and Aβ plaque formation, and concomitantly ameliorated spatial learning and memory deficits examined in Y-maze and Morris water maze tests. Moreover, in parallel with reducing apoptosis and neural loss in the hippocampal subfields, IFNβ decreased ectopic neurogenesis in the CA1 and CA3 regions of the AD rat hippocampus. However, IFNβ increased neurogenesis in the dentate gyrus neurogenic niche. Our findings suggest that IFNβ exerts neuroprotective effects at least partly by inhibition of apoptosis and modulation of neurogenesis. Taken together, IFNβ can be a promising therapeutic approach to improve cognitive performance in AD-like neurodegenerative context.

journal_name

Prog Neuropsychopharmacol Biol Psychiatry

journal_title

Progress in neuro-psychopharmacology & biological psychiatry

authors

Chavoshinezhad S,Mohseni Kouchesfahani H,Ahmadiani A,Dargahi L

doi

10.1016/j.pnpbp.2019.109661

subject

Has Abstract

pub_date

2019-08-30 00:00:00

pages

109661

eissn

0278-5846

issn

1878-4216

pii

S0278-5846(19)30089-2

journal_volume

94

pub_type

杂志文章

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