Related Experiment Videos
Liver Dysfunction as a Novel Player in Alzheimer's Progression: Looking Outside the Brain
Lisbell D Estrada1, Pablo Ahumada1, Daniel Cabrera1,2
1Bionanotechnology Laboratory, Integrative Center for Applied Biology and Chemistry (CIBQA), Department of Chemical & Biological Sciences, Universidad Bernardo O'Higgins, Santiago, Chile.
Frontiers in Aging Neuroscience
|August 6, 2019
Summary
Nonalcoholic fatty liver disease (NAFLD) may influence Alzheimer's disease (AD) by impairing the clearance of amyloid-beta (Aβ) peptides. The LRP-1 receptor, crucial for Aβ clearance, is implicated in both NAFLD and AD.
Area of Science:
- Neuroscience
- Hepatology
- Pathology
Background:
- Alzheimer's disease (AD) is a leading cause of dementia, characterized by amyloid plaques and neurofibrillary tangles.
- Amyloid-beta (Aβ) oligomers contribute to synaptic loss and cognitive decline in AD.
- The blood-brain barrier (BBB) is impaired in AD, affecting substance clearance.
Purpose of the Study:
- To review the literature linking nonalcoholic fatty liver disease (NAFLD) and AD.
- To investigate the role of impaired peripheral clearance in AD pathogenesis.
- To highlight the function of the LRP-1 receptor in Aβ clearance in both conditions.
Main Methods:
- Literature review of studies on NAFLD, AD, and Aβ clearance.
- Examination of the role of the blood-brain barrier (BBB) in AD.
- Focus on the LRP-1 receptor's involvement in hepatic and cerebral Aβ efflux.
Main Results:
- NAFLD is prevalent and characterized by impaired peripheral clearance.
- BBB impairment is observed in AD patients and models.
- The LRP-1 receptor is a key protein for Aβ clearance, expressed in the liver, brain, and vasculature.
Conclusions:
- Impaired peripheral clearance, as seen in NAFLD, may contribute to Aβ accumulation in AD.
- The LRP-1 receptor is a potential link between NAFLD and AD pathogenesis.
- Further investigation is needed to understand the impact of BBB and peripheral clearance on AD.