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Updated: Jan 27, 2026

In Vitro Aggregation Assays Using Hyperphosphorylated Tau Protein
Published on: January 2, 2015
Antimicrobial peptides inhibit Tau aggregation and modulates its pathology
Subashchandrabose Chinnathambi1, Nagaraj Rangappa1, Sneha Malik1
1Department of Neurochemistry, National Institute of Mental Health and Neuro Sciences, Institute of National Importance, Bangalore, Karnataka, India.
Abstract:
Alzheimer's disease is mainly caused by two proteins, Tau and Amyloid-β. While there are several cures currently being explored for it, there is no cure yet for the disease progression and prevention, but only those to alleviate the symptoms. One of the hypothesis for the cause of the Alzheimer's disease is the microbial hypothesis. This suggests that there are a lot of microorganisms present in our body which can contribute to the disease pathology by leading to symptoms such as neuroinflammation. Our body has certain molecules to maintain innate immunity, known as antimicrobial peptides. Recently, several studies suggest the roles of these molecules in the Alzheimer's disease as therapeutic molecules and as biomarkers. Amyloid beta which is one of the major proteins is suggested to be an antimicrobial peptide on its own. The formation of its oligomers and plaques is due to neuroprotective reasons. A similar theory exists for the formation of neurofibrillary tangles (NFTs) from Tau. There include lactoferrin, LL-37 and defensins. They are often found in association with the aggregated proteins, amyloid beta and Tau. Additionally, fluctuations in their levels are often observed in several fluids and regions inside in patients with AD compared to the control cohorts. While their therapeutic potential has been proven, their mechanisms of action, effectivity and expedition towards clinical studies is yet to be done.
Insights
Antimicrobial peptides may play a role in Alzheimer's disease (AD) pathology, potentially offering new therapeutic avenues. Research suggests these molecules, including amyloid beta, are involved in neuroinflammation and protein aggregation in AD patients.
Area of Science:
- Neuroscience
- Immunology
- Microbiology
Background:
- Alzheimer's disease (AD) pathology involves Tau and Amyloid-beta proteins, with no current cure for disease progression.
- The microbial hypothesis suggests microorganisms contribute to AD via neuroinflammation.
- Antimicrobial peptides are key to innate immunity and are increasingly studied in AD.
Purpose of the Study:
- To explore the role of antimicrobial peptides in Alzheimer's disease.
- To investigate antimicrobial peptides as potential biomarkers and therapeutic agents for AD.
- To understand the connection between antimicrobial peptides, amyloid beta, and Tau in AD.
Main Methods:
- Literature review of studies on antimicrobial peptides in Alzheimer's disease.
- Analysis of research linking antimicrobial peptides to amyloid beta and Tau aggregation.
- Examination of studies reporting altered antimicrobial peptide levels in AD patients.
Main Results:
- Amyloid beta may function as an antimicrobial peptide, with aggregation potentially being a neuroprotective response.
- Other antimicrobial peptides like lactoferrin, LL-37, and defensins are found with aggregated proteins.
- Fluctuating levels of these peptides are observed in AD patients compared to controls.
Conclusions:
- Antimicrobial peptides are implicated in Alzheimer's disease pathogenesis and progression.
- These peptides show therapeutic potential and can serve as biomarkers for AD.
- Further clinical studies are needed to determine their mechanisms, efficacy, and application in AD treatment.
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