Amyloid-β, BACE, and oxidative stress in Alzheimer's disease, a commentary on “The different aggregation state of beta-amyloid 1-42 mediates different effects on oxidative stress, neurodegeneration and BACE-1 expression”

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) triggered the pandemic Coronavirus Disease 19 (COVID-19), causing millions of deaths. The elderly and those already living with comorbidity are likely to die after SARS-CoV-2 infection. People suffering from Alzheimer’s disease (AD) have a higher risk of becoming infected, because they cannot easily follow health roles. Additionally, those suffering from dementia have a 40% higher risk of dying from COVID-19. Herein, we collected from Gene Expression Omnibus repository the brain samples of AD patients who died of COVID-19 (AD+COVID-19), AD without COVID-19 (AD), COVID-19 without AD (COVID-19) and control individuals. We inspected the transcriptomic and interactomic profiles by comparing the COVID-19 cohort against the control cohort and the AD cohort against the AD+COVID-19 cohort. SARS-CoV-2 in patients without AD mainly activated processes related to immune response and cell cycle. Conversely, 21 key nodes in the interactome are deregulated in AD. Interestingly, some of them are linked to beta-amyloid production and clearance. Thus, we inspected their role, along with their interactors, using the gene ontologies of the biological process that reveals their contribution in brain organization, immune response, oxidative stress and viral replication. We conclude that SARS-CoV-2 worsens the AD condition by increasing neurotoxicity, due to higher levels of beta-amyloid, inflammation and oxidative stress.

Download Full-text

The Glutamatergic System in Alzheimer’s Disease Brain: Dysfunction Associated with Amyloid β-Peptide and Oxidative Stress

Excitotoxicity in Neurological Diseases ◽

10.1007/978-1-4419-8959-8_14 ◽

2004 ◽

pp. 251-262 ◽

Cited By ~ 2

Author(s):

D. Allan Butterfield

Keyword(s):

Oxidative Stress ◽

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Amyloid Β ◽

Brain Dysfunction ◽

Amyloid Β Peptide ◽

Glutamatergic System ◽

And Oxidative Stress

Download Full-text

P4-283: High levels of BETA-AMYLOID and oxidative stress with no evidence of Alzheimer's disease-like pathology in the longest-lived rodent

Alzheimer s & Dementia ◽

10.1016/j.jalz.2013.08.064 ◽

2012 ◽

Vol 8 (4S_Part_21) ◽

pp. S757-S757

Author(s):

Yael Edrey ◽

Antonella Caccamo ◽

Salvatore Oddo ◽

Rochelle Buffenstein

Keyword(s):

Oxidative Stress ◽

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Beta Amyloid ◽

And Oxidative Stress

Download Full-text

Faculty Opinions recommendation of A copper-binding site in the cytoplasmic domain of BACE1 identifies a possible link to metal homoeostasis and oxidative stress in Alzheimer's disease.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1089777.542917 ◽

2007 ◽

Author(s):

George Perry

Keyword(s):

Oxidative Stress ◽

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Binding Site ◽

Cytoplasmic Domain ◽

Copper Binding ◽

And Oxidative Stress

Download Full-text

Alpha-1-Antichymotrypsin: a Common Player for Type 2 Diabetes and Alzheimer's Disease

Current Diabetes Reviews ◽

10.2174/1573399816999201012200537 ◽

2020 ◽

Vol 16 ◽

Author(s):

Nataly Guzmán-Herrera ◽

Viridiana C. Pérez-Nájera ◽

Luis A. Salazar-Olivo

Keyword(s):

Oxidative Stress ◽

Alzheimer’S Disease ◽

Type 2 Diabetes ◽

Alzheimer's Disease ◽

Regulatory Networks ◽

Therapeutic Strategies ◽

Oxidative Stresses ◽

Bibliographic Search ◽

And Oxidative Stress

Background: Numerous studies have shown a significant association between type 2 diabetes mellitus (T2D) and Alzheimer's disease (AD), two pathologies affecting millions of people worldwide. Chronic inflammation and oxidative stress are two conditions common to these diseases also affecting the activity of the serpin alpha-1-antichymotrypsin (ACT), but a possible common role for this serpin in T2D and AD remains unclear. Objective: To explore the possible regulatory networks linking ACT to T2D and AD. Materials and Methods: A bibliographic search was carried out in PubMed, Med-line, Open-i, ScienceDirect, Scopus and SpringerLink for data indicating or suggesting association among T2D, AD, and ACT. Searched terms like “alpha-1-antichymotrypsin”, “type 2 diabetes”, “Alzheimer's disease”, “oxidative stress”, “pro-inflammatory mediators” among others were used. Moreover, common therapeutic strategies between T2D and AD as well as the use of ACT as a therapeutic target for both diseases were included. Results: ACT has been linked with development and maintenance of T2D and AD and studies suggest their participation through activation of inflammatory pathways and oxidative stress, mechanisms also associated with both diseases. Likewise, evidences indicate that diverse therapeutic approaches are common to both diseases. Conclusion: Inflammatory and oxidative stresses constitute a crossroad for T2D and AD where ACT could play an important role. In-depth research on ACT involvement in these two dysfunctions could generate new therapeutic strategies for T2D and AD.

Download Full-text