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Molecular Links Between Alzheimer's Disease and Gastrointestinal Microbiota: Emphasis on Helicobacter pylori
Taxiarchis Katsinelos1, Michael Doulberis2,3, Stergios A Polyzos3,4
1UK Dementia Research Institute at the University of Cambridge, Hills Road, Cambridge, CB2 0AH, United Kingdom.
Abstract:
Alzheimer's disease (AD) is a neurodegenerative disease and the main form of dementia, characterized by progressive cognitive decline and detrimental consequences in both personal-family and global level. Within this narrative review, we provide recent molecular aspects of Tau, a microtubule AD-associated protein, as well as amyloid beta, involved in AD pathophysiology. Moreover, we provide additional emerging data from basic research as well as clinical studies indicating an implicating role of gastrointestinal microbiota (GI-M), including Helicobacter pylori infection (Hp-I), in AD pathophysiology. Likewise, we identified through a molecular prism the current evidence of AD pathogenesis as well as its linkage with GI-M and emphasizing the role of Hp-I. All in all, additional large-scale studies are required for the further clarification of AD pathophysiology and its connection with GI-M and Hp-I, so as novel therapies on molecular basis become available.
Insights
Alzheimer's disease (AD) involves Tau and amyloid beta proteins. Emerging research links gastrointestinal microbiota, including Helicobacter pylori infection, to AD, suggesting new therapeutic targets.
Area of Science:
- Neuroscience
- Gastroenterology
- Microbiology
Background:
- Alzheimer's disease (AD) is a leading cause of dementia, marked by cognitive decline.
- Key molecular players include Tau proteins and amyloid beta.
- The gut microbiome's role in neurodegenerative diseases is an emerging area of research.
Purpose of the Study:
- To review molecular aspects of Tau and amyloid beta in AD.
- To explore the emerging role of gastrointestinal microbiota (GI-M) in AD.
- To examine the specific link between Helicobacter pylori infection (Hp-I) and AD.
Main Methods:
- This is a narrative review of existing literature.
- Molecular mechanisms of AD pathogenesis were analyzed.
- Evidence linking GI-M and Hp-I to AD was synthesized.
Main Results:
- Review confirms Tau and amyloid beta's established roles in AD.
- Emerging data suggests GI-M influences AD pathophysiology.
- Helicobacter pylori infection is implicated as a potential factor in AD.
Conclusions:
- Further large-scale studies are needed to clarify AD's connection with GI-M and Hp-I.
- Understanding these links may reveal novel molecular-based therapies for AD.
- Investigating the gut-brain axis offers promising avenues for AD research.