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Pharmacol Rep. 2015 Apr;67(2):326-31. doi: 10.1016/j.pharep.2014.09.013. Epub 2014 Oct 16.

Study of the protective effects of nootropic agents against neuronal damage induced by amyloid-beta (fragment 25-35) in cultured hippocampal neurons.

Author information

1
Department of Pediatric Neurology and Rehabilitation, Medical University of Bialystok, Białystok, Poland. Electronic address: krsen@wp.pl.
2
Department of Pediatric Neurology and Rehabilitation, Medical University of Bialystok, Białystok, Poland.
3
Department of Immunology, Medical University of Bialystok, Białystok, Poland.
4
Department of Pediatric Orthopedics and Traumatology, Medical University of Bialystok, Białystok, Poland.

Abstract

BACKGROUND:

Alzheimer's disease (AD) is a common neurodegenerative disorder, in which progressive neuron loss, mainly in the hippocampus, is observed. The critical events in the pathogenesis of AD are associated with accumulation of β-amyloid (Aβ) peptides in the brain. Deposits of Aβ initiate a neurotoxic "cascade" leading to apoptotic death of neurons. Aim of this study was to assess a putative neuroprotective effects of two nootropic drugs: piracetam (PIR) and levetiracetam (LEV) on Aβ-injured hippocampal neurons in culture.

METHODS:

Primary cultures of rat's hippocampal neurons at 7 day in vitro were exposed to Aβ(25-35) in the presence or absence of nootropics in varied concentrations. Flow cytometry with Annexin V/PI staining was used for counting and establishing neurons as viable, necrotic or apoptotic. Additionally, release of lactate dehydrogenase (LDH) to the culture medium, as a marker of cell death, was evaluated.

RESULTS:

Aβ(25-35) caused concentration-dependent death of about one third number of hippocampal neurons, mainly through an apoptotic pathway. In drugs-containing cultures, number of neurons injured with 20 μM Aβ(25-35) was about one-third lesser for PIR and almost two-fold lesser for LEV. When 40 μM Aβ(25-35) was used, only LEV exerted beneficial neuroprotective action, while PIR was ineffective.

CONCLUSIONS:

Our results suggest the protective potential of both studied nootropics against Aβ-induced death of cultured hippocampal neurons with more powerful neuroprotective effects of LEV.

KEYWORDS:

Hippocampal culture; Neuroprotection; Nootropic drugs; β-Amyloid

PMID:
25712658
DOI:
10.1016/j.pharep.2014.09.013
[Indexed for MEDLINE]

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