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Early β-Amyloid-induced Synaptic Dysfunction Is Counteracted by Estrogen in Organotypic Hippocampal Cultures.

Abstract：

:In the present study we set up a model of slow progression of neuronal injury by exposing organotypic hippocampal cultures to a low concentration of Amyloid β (25-35) peptide (Aβ, 2 μM) to analyze the time-related effects of 17-β estradiol (17β-E2, 10 nM). Neuronal death occurs after 7 d and is prevented by addition of 17β-E2 24 h prior to, together with or 48 h after exposure to Aβ. This effect is mimicked by selective ERα agonist PPT (100 nM). Treatment with Aβ leads to early and transient (16-72 h) increase of pre- and post-synaptic proteins synaptophysin and PSD95, followed by a decrease coincident with neuronal death (7d), all prevented by 17β-E2. At 72 h of Aβ exposure, synaptic activity is increased, as by higher levels of glutamate and increased loading and unloading of FM 1-43-labeled synaptic vesicles. All these effects are also prevented by 17β-E2. These data point out beneficial effects of estrogen on early Aβ-induced synaptic disruption.

journal_name

Curr Alzheimer Res

journal_title

Current Alzheimer research

authors

Merlo S,Spampinato SF,Capani F,Sortino MA

doi

10.2174/1567205013666160125113509

subject

Has Abstract

pub_date

2016-01-01 00:00:00

pages

631-40

issue

6

eissn

1567-2050

issn

1875-5828

pii

CAR-EPUB-73205

journal_volume

13

pub_type

杂志文章

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