Az öregedés fokozza az amiloid prekurzor protein és a triptofán 2,3-dioxigenáz gének transzkripció ját patkányagyban

Translated title of the contribution: The transcription of the amyloid precursor protein and tryptophan 2,3-dioxygenase genes are increased by aging in the rat brain

Sára Kálmán, M. Pákáski, Szabina Szucs, Dénes Garab, Ágnes Domokos, A. Zvara, L. Puskás, G. Bagdy, D. Zelena, J. Kálmán

Research output: Contribution to journalArticle

Abstract

Aging itself is considered as a major risk factor of dementia. The prevalence of the Alzheimer's disease (AD) is increasing exponentially after the age of 65 and doubles every 5 years. The major aim of our present research was to examine the effect of aging on the transcription of certain genes associated with neurodegenerative disorders in the rat brain. The influence of the vasopressin (VP) hormone was also examined in the same experimental paradigm. Age dependent transcriptional changes of the following four genes were examined in the cerebral cortex: the first was the gene of the amyloid precursor protein (APP) which is abnormally cleaved to toxic beta-amyloid fragments. These aggregated peptides are the major components of the senile plaques in the AD brain. The second one was the mitogen-activated protein kinase (MAPK1) gene. The MAPK is involved in the abnormal hyperphosphorylation of the tau-protein which results in aggregated neurofibrillary tangles. The beta-actin gene was the third one. The protein product of this gene is considered to be involved in synaptogenesis, neuronal plasticity and clinical conditions like depression and AD. The last one was the gene of the tryptophan 2,3-dioxygenase (TDO2) enzyme. The activity of this enzyme is considered as a rate limiting factor in the metabolism of the neuro-immune modulator quinolinic acid (QUIN). The transciptional activity of young (2.5 months) and aged (13 months) Brattleboro rats with or without VP expression were compared by means of real time PCR technique. The cortical transciptional activity of the APP and TDO2 genes were increased in the aged animals as compared with the activity of the young ones, and this effect was independent on the presence of the VR Our results indicate the importance of certain age dependent transcriptional changes might influence the mechanism of AD and other neurodegenerative disorders.

Original languageHungarian
Pages (from-to)326-332
Number of pages7
JournalIdeggyógyászati szemle
Volume62
Issue number9-10
Publication statusPublished - Sep 30 2009

Fingerprint

Tryptophan Oxygenase
Amyloid beta-Protein Precursor
Brain
Alzheimer Disease
Genes
Vasopressins
Neurodegenerative Diseases
Brattleboro Rats
Quinolinic Acid
tau Proteins
Neurofibrillary Tangles
Neuronal Plasticity
Poisons
Mitogen-Activated Protein Kinase 1
Amyloid Plaques
Enzymes
Amyloid
Cerebral Cortex
Dementia
Actins

ASJC Scopus subject areas

  • Clinical Neurology
  • Neurology

Cite this

Az öregedés fokozza az amiloid prekurzor protein és a triptofán 2,3-dioxigenáz gének transzkripció ját patkányagyban. / Kálmán, Sára; Pákáski, M.; Szucs, Szabina; Garab, Dénes; Domokos, Ágnes; Zvara, A.; Puskás, L.; Bagdy, G.; Zelena, D.; Kálmán, J.

In: Ideggyógyászati szemle, Vol. 62, No. 9-10, 30.09.2009, p. 326-332.

Research output: Contribution to journalArticle

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