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Subject: search.filters.subject.Alzheimer's disease

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    Neonatal Neurodegeneration in Alzheimer's Disease Transgenic Mouse Model
    (IOS PRESS, 2018-01-01) Mazi, Aise Rumeysa; Arzuman, Aysegul Sumeyye; Gurel, Busra; Sahin, Betul; Tuzuner, Mete Bora; Ozansoy, Mehmet; Baykal, Ahmet Tarik
    Alzheimer's disease (AD) is a progressive disorder characterized by a variety of molecular pathologies causing cortical dementia with a prominent memory deficit. Formation of the pathology, which begins decades before the diagnosis of the disease, is highly correlated with the clinical symptoms. Several proteomics studies were performed using animal models to monitor the alterations of the brain tissue proteome at different stages of AD. However, proteome changes in the brain regions of newborn transgenic mouse model have not been investigated yet. To this end, we analyzed protein expression alterations in cortex, hippocampus and cerebellum of transgenic mice carrying five familial AD mutations (5XFAD) at neonatal day-1. Our results indicate a remarkable difference in protein expression profile of newborn 5XFAD brain with region specific variations. Additionally, the proteins, which show similar expression alteration pattern in postmortem human AD brains, were determined. Bioinformatics analysis showed that the molecular alterations were mostly related to the cell morphology, cellular assembly and organization, and neuroinflammation. Moreover, morphological analysis revealed that there is an increase in neurite number of 5XFAD mouse neurons in vitro. We suggest that, molecular alterations in the AD brain exist even at birth, and perhaps the disease is silenced until older ages when the brain becomes vulnerable.
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    Self-perspective Versus Caregiver-perspective on Cognitive Impairment at Different Stages of the Alzheimer's Continuum
    (GALENOS PUBL HOUSE, 2022-01-01) Seckin, Mustafa; Ozturk, Gulcan; Dilmac, Ecem; Gurvit, Hakan
    Objective: To understand how the patients' and their study partners'/caregivers' perspectives on cognitive decline change at the subjective cognitive decline (SCD), mild cognitive impairment (MCI), and probable Alzheimer's disease (PRAD) stages of the Alzheimer's disease (AD) continuum. Materials and Methods: Twenty-three individuals with the diagnosis of SCD, 33 individuals with the diagnosis of MCI, and 17 individuals with the diagnosis of PRAD were included. A cognitive testing battery including the standardized mini-mental state examination (MMSE), digit span forward and backwards tests, and the semantic fluency test were administered to all patients. The cognitive function instrument (CFI) was used for the subjective assessment of cognitive decline. The same questions in the CFI were answered both by the patients (CFI-self report) and the study partners (CFI-partner report). Results: In the SCD and the MCI groups, the CFI-self report scores were higher than the CFI-partner report scores, whereas an opposite pattern was found in the PRAD group with higher CFI-partner report scores and lower CFI-self report scores. The CFI self report scores positively correlated with the MMSE scores in the PRAD group showing higher ratings in cognitively less impaired individuals, and vice versa. The CFI partner-report scores did not show a significant correlation with the MMSE scores in any of the groups, however a trend for a negative correlation was observed in the MCI group. Finally, the CFI-self report and partner report scores significantly correlated only in the MCI group. Conclusion: Report-based assessment of cognitive decline can be informative, particularly in the early stages of the AD continuum. However, the loss of insight in PRAD may mask the symptoms when the subjective cognitive assessment relies on the patients' perspective. The greatest concordance between the patients' and their partners' perspectives was evident in the MCI stage which represented a transitional period between SCD and PRAD.
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    Brain region-specific amyloid plaque-associated myelin lipid loss, APOE deposition and disruption of the myelin sheath in familial Alzheimer's disease mice
    (WILEY, 2020-01-01) Kaya, Ibrahim; Jennische, Eva; Lange, Stefan; Baykal, Ahmet Tarik; Malmberg, Per; Fletcher, John S.
    There is emerging evidence that amyloid beta (A beta) aggregates forming neuritic plaques lead to impairment of the lipid-rich myelin sheath and glia. In this study, we examined focal myelin lipid alterations and the disruption of the myelin sheath associated with amyloid plaques in a widely used familial Alzheimer's disease (AD) mouse model