Alterations in the <em>amyloid protein precursor</em>, <em>α-secretase</em>, <em>β-secretase</em>, <em>presenilins</em> and <em>tau protein</em> Genes in the CA3 Area of the Hippocampus in a 2-Year Ischemic Model of Alzheimer’s Disease DOI Open Access
Stanisław J. Czuczwar, Janusz Kocki, Barbara Miziak

и другие.

Опубликована: Сен. 30, 2023

Understanding the phenomena underlying non-selective susceptibility to ischemia of py-ramidal neurons in CA3 area hippocampus is important from point view elu-cidating mechanisms memory loss and development post-ischemic dementia. We used an ischemic model Alzheimer's disease study changes amyloid protein precursor gene expression, its cleavage enzymes tau af-ter a 10-minute brain with 12, 18, 24-month survival. Quantitative reverse tran-scriptase PCR assay showed that expression all genes contribute pro-duction was dysregulated within 2 years after ischemia. The above control values at times study. &alpha;-secretase also exceeded throughout In contrast, &beta;-secretase reaching maximum increase 12 months ischemia, below 18 again 24 Presenilin 1 significantly elevated follow-up period, peak both occurring This suggests studied are involved non-amyloidogenic processing precursor. Also, observation present is-chemia. Data indicate episode long-term survival causes damage death pyramidal manner dependent on modified protein. Thus defining new mechanism neuronal addition modification is-chemia useful identifying disease.

Язык: Английский

Alterations in the <em>amyloid protein precursor</em>, <em>α-secretase</em>, <em>β-secretase</em>, <em>presenilins</em> and <em>tau protein</em> Genes in the CA3 Area of the Hippocampus in a 2-Year Ischemic Model of Alzheimer’s Disease DOI Open Access
Stanisław J. Czuczwar, Janusz Kocki, Barbara Miziak

и другие.

Опубликована: Сен. 30, 2023

Understanding the phenomena underlying non-selective susceptibility to ischemia of py-ramidal neurons in CA3 area hippocampus is important from point view elu-cidating mechanisms memory loss and development post-ischemic dementia. We used an ischemic model Alzheimer's disease study changes amyloid protein precursor gene expression, its cleavage enzymes tau af-ter a 10-minute brain with 12, 18, 24-month survival. Quantitative reverse tran-scriptase PCR assay showed that expression all genes contribute pro-duction was dysregulated within 2 years after ischemia. The above control values at times study. &alpha;-secretase also exceeded throughout In contrast, &beta;-secretase reaching maximum increase 12 months ischemia, below 18 again 24 Presenilin 1 significantly elevated follow-up period, peak both occurring This suggests studied are involved non-amyloidogenic processing precursor. Also, observation present is-chemia. Data indicate episode long-term survival causes damage death pyramidal manner dependent on modified protein. Thus defining new mechanism neuronal addition modification is-chemia useful identifying disease.

Язык: Английский

Процитировано

1