Browsing by Author "Karoğlu, Elif Tuğçe"

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Open Access
Age and gender alter synaptic proteins in zebrafish (Danio Rerio) models of normal and delayed aging
(2017-07) Karoğlu, Elif Tuğçe
Cognitive decline occurs during normal aging in some specific domains of cognitive abilities including but not limited to episodic memory, divided attention and executive functions, however, it is not a unitary decline since some cognitive domains, including vocabulary and implicit memory tend to be preserved and even improved at older ages. Normal aging is not associated with global and significant neuronal and synapse loss, yet subtle molecular alterations occurring in gene expression patterns, protein homeostasis, mitochondrial dynamics and hypofunction in the cholinergic system may account for the age related decline in some cognitive abilities. Additionally, males and females showed differential vulnerabilities against age-related alterations in the cognitive abilities, physiological integrity and subtle molecular dynamics. More direct relationships can be established between the age-related cognitive decline and subtle molecular changes by analyzing the elements of synaptic integrity, which could alter synaptic plasticity and result in the changes in learning and memory abilities. Post-synaptic 95 (PSD-95), gephyrin (GEP) and synaptophysin (SYP) are integral synaptic proteins and they could be attributed as indicators of excitatory post-synaptic, inhibitory post-synaptic and pre-synaptic integrities, respectively. The first aim of this study was to show effects of age and gender on the expression levels of PSD-95, GEP and SYP in young, middle-aged and old, female and male zebrafish cohorts. Significant age by gender interactions were revealed in the levels of PSD-95 and SYP. It was shown that PSD-95 and SYP levels tend to be preserved and increased in the female groups throughout the aging process, whereas, in male groups, expression levels of these proteins tend to be reduced at older ages. The second aim was to investigate whether ameliorating the cholinergic hypofunction might have beneficial effects on the aging-related protein expression alterations and check for sexually dimorphic patterns. For this aim old male and female zebrafish from a mutant line (ache), which has decreased levels of acetylcholinesterase and increased levels of acetylcholine, were compared with old male and female wildtype animals. In the ache old groups, significant increases in the expression levels of SYP and GEP were revealed compared to the wildtype, and also in the old ache females SYP expression was higher than the other groups. These studies emphasized the importance of gender and sexually dimorphic patterns in the context of aging andcholinergic manipulations could be a promising target of intervention to attenuate the effects of age-related synaptic alterations, which could have possible contributions to age-related cognitive decline. .
Open Access
Mammalian target of rapamycin (mTOR), aging, neuroscience, and their association with aging-related diseases
(Elsevier Inc., 2016) Celebi-Birand, Ergül Dilan; Karoğlu, Elif Tuğçe; Doldur-Ballı, Füsun; Adams, Michelle M.; Maiese, K.
Normal aging is accompanied by cognitive impairment with subtle cellular and molecular changes in the brain, whereas, pathological brain aging manifests as severe behavioral impairments with cellular pathology. Understanding the factors that contribute to both states is undoubtedly important for determining appropriate interventions that alter their progression. Mammalian target of rapamycin (mTOR) signaling has been implicated in affecting lifespan and age-related diseases such as cancer. The relationship of mTOR signaling with pathological brain aging has been more extensively studied, whereas the association with normal brain aging is not well understood. In this chapter we present information about normal and pathological brain aging, the relationship with mTOR signaling and use information from other age-related diseases to suggest that mTOR may have a role in promoting the cellular and molecular changes that underlie age-related cognitive changes. Future work should be directed towards understanding the precise role of mTOR signaling in brain aging. © 2016 Elsevier Inc. All rights reserved.