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Published on: December 26, 2016
Macrophages in Alzheimer's disease: the blood-borne identity
David Gate1, Kavon Rezai-Zadeh, Dominique Jodry
1Department of Biomedical Sciences, Regenerative Medicine Institute, Cedars-Sinai Medical Center, 8700 Beverly Blvd., Steven Spielberg Building, Room 361, Los Angeles, CA 90048, USA.
Abstract:
Alzheimer's disease (AD) is a progressive and incurable neurodegenerative disorder clinically characterized by cognitive decline involving loss of memory, reasoning and linguistic ability. The amyloid cascade hypothesis holds that mismetabolism and aggregation of neurotoxic amyloid-beta (Abeta) peptides, which are deposited as amyloid plaques, are the central etiological events in AD. Recent evidence from AD mouse models suggests that blood-borne mononuclear phagocytes are capable of infiltrating the brain and restricting beta-amyloid plaques, thereby limiting disease progression. These observations raise at least three key questions: (1) what is the cell of origin for macrophages in the AD brain, (2) do blood-borne macrophages impact the pathophysiology of AD and (3) could these enigmatic cells be therapeutically targeted to curb cerebral amyloidosis and thereby slow disease progression? This review begins with a historical perspective of peripheral mononuclear phagocytes in AD, and moves on to critically consider the controversy surrounding their identity as distinct from brain-resident microglia and their potential impact on AD pathology.
Insights
Blood-borne macrophages may infiltrate the Alzheimer's disease (AD) brain, potentially restricting amyloid plaques. Further research is needed to understand their origin and therapeutic potential in curbing AD pathology.
Area of Science:
- Neuroscience
- Immunology
- Pathology
Background:
- Alzheimer's disease (AD) is a progressive neurodegenerative disorder marked by cognitive decline.
- The amyloid cascade hypothesis implicates amyloid-beta (Abeta) peptide aggregation in AD etiology.
- Emerging evidence suggests peripheral macrophages may influence AD pathology.
Purpose of the Study:
- To review the role of blood-borne mononuclear phagocytes in Alzheimer's disease.
- To investigate the origin and function of macrophages within the AD brain.
- To explore the therapeutic potential of targeting these cells for AD treatment.
Main Methods:
- Literature review and critical analysis of existing studies.
- Historical perspective on peripheral mononuclear phagocytes in AD research.
- Examination of evidence from AD mouse models.
Main Results:
- Blood-borne mononuclear phagocytes show potential for brain infiltration in AD models.
- These cells may restrict amyloid plaque deposition, impacting disease progression.
- Controversy exists regarding their distinction from brain-resident microglia.
Conclusions:
- The origin and precise role of peripheral macrophages in the AD brain require further elucidation.
- Understanding these cells could reveal novel therapeutic targets for Alzheimer's disease.
- Targeting blood-borne macrophages may offer a strategy to reduce cerebral amyloidosis.
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