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Inflammopharmacology

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01.06.2020 | Original Article

Perindopril ameliorates experimental Alzheimer’s disease progression: role of amyloid β degradation, central estrogen receptor and hyperlipidemic-lipid raft signaling

verfasst von: Basim A. S. Messiha, Mohammed R. A. Ali, Mahmoud M. Khattab, Amira M. Abo-Youssef

Erschienen in: Inflammopharmacology | Ausgabe 5/2020

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Abstract

Accumulating evidence indicates that over-stimulation of angiotensin-converting enzyme 1 (ACE1) activity is associated with β-amyloid (Aβ) and phosphorylated tau (p-tau)-induced apoptosis, oxido-nitrosative neuroinflammatory stress and neurodegeneration in Alzheimer’s disease (AD). Alternatively, activation of the ACE2, the metalloprotease neprilysin (Neutral Endopeptidase; NEP) and the insulin-degrading enzyme (IDE) could oppose the effects of ACE1 activation. We aim to investigate the relationship between ACE1/ACE2/NEP/IDE and amyloidogenic/hyperlipidemic-lipid raft signaling in hyperlipidemic AD model. Induction of AD was performed in ovariectomized female rats with high-fat high fructose diet (HFFD) feeding after 4 weeks following d-galactose injection (150 mg/kg). The brain-penetrating ACE1 inhibitor perindopril (0.5 mg/kg/day, p.o.) was administered on a daily basis for 30 days. Perindopril significantly decreased hippocampal expression of ACE1 and increased expression of ACE2, NEP and IDE. Perindopril markedly decreased Aβ_1–42, improved lipid profile and ameliorated the lipid raft protein markers caveolin1 (CAV1) and flotillin 1 (FLOT1). This was accompanied by decreased expression of p-tau and enhancement of cholinergic neurotransmission, coupled with decreased oxido-nitrosative neuroinflammatory stress, enhancement of blood–brain barrier (BBB) functioning and lower expression of the apoptotic markers glial fibrillary acidic protein (GFAP), Bax and β-tubulin. In addition, perindopril ameliorated histopathological damage and improved learning, cognitive and recognition impairment as well as depressive behavior in Morris water maze, Y maze, novel object recognition and forced swimming tests, respectively. Conclusively, perindopril could improve cognitive defects in AD rats, at least through activation of ACE2/NEP/IDE and inhibition of ACE1 and subsequent modulation of amyloidogenic/hyperlipidemic-lipid raft signaling and oxido-nitrosative stress.

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Titel: Perindopril ameliorates experimental Alzheimer’s disease progression: role of amyloid β degradation, central estrogen receptor and hyperlipidemic-lipid raft signaling
verfasst von: Basim A. S. Messiha
Mohammed R. A. Ali
Mahmoud M. Khattab
Amira M. Abo-Youssef
Publikationsdatum: 01.06.2020
Verlag: Springer International Publishing
Erschienen in: Inflammopharmacology / Ausgabe 5/2020
Print ISSN: 0925-4692
Elektronische ISSN: 1568-5608
DOI: https://doi.org/10.1007/s10787-020-00724-4

Die Highlights vom Kongress des American College of Cardiology 2024

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Perindopril ameliorates experimental Alzheimer’s disease progression: role of amyloid β degradation, central estrogen receptor and hyperlipidemic-lipid raft signaling

Abstract

Die Highlights vom Kongress des American College of Cardiology 2024

Springer Medizin

Abstract

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