Abstract
Alzheimer's disease (AD) is the most common form of dementia, which is characterized by a progressive cognitive decline and senile plaques formed by amyloid β (Aβ). Microglia are the immune cells of the central nervous system (CNS). Studies have proposed 2 types of microglia, namely, the resident microglia and bone marrow-derived microglia (BMDM). Recent studies suggested that BMDM, not the resident microglia, can phagocytose Aβ, which has a great therapeutic potential in AD. Bone marrow-derived microglia can populate the CNS in an efficient manner and their functions can be regulated by some genes. Thus, methods that increase their recruitment and phagocytosis could be used as a new tool that clears Aβ and ameliorates cognitive impairment. Herein, we review the neuroprotective functions of BMDM and their therapeutic potential in AD.
Highlights
Alzheimer’s disease (AD) is the most common form of dementia worldwide, affecting 50 million people approximately.[1]
CCchemokine receptor 2 (CCR2) is one of the chemokine receptors that bind to CC-chemokine ligand 2 (CCL2), which is essential in the process of monocyte mobilizing from the bone marrow and engrafting to inflammatory sites in AD.[22]
Their study showed that bone marrow–derived macrophages derived from ATP-binding cassette transporter A7 (ABCA7)-deficient mice had a 51% reduction in the ability to take up oligomeric amyloid b (Ab) compared to wild-type mice.[43]
Summary
Alzheimer’s disease (AD) is the most common form of dementia worldwide, affecting 50 million people approximately.[1]. CCchemokine receptor 2 (CCR2) is one of the chemokine receptors that bind to CC-chemokine ligand 2 (CCL2), which is essential in the process of monocyte mobilizing from the bone marrow and engrafting to inflammatory sites in AD.[22] When Tg2576 mice with AD were crossed with (CCR2À/À) mice, blood-derived monocytic cells were fewer, indicating that the CCR2-dependent infiltration of blood-derived monocytic cells may exist in AD.[23] Recent studies have demonstrated that the CCL2/CCR2 pathway affects the migration of monocytes in some inflammation models such as sterile peritonitis, atherosclerosis, and Listeria infection,[24] suggesting that the same process may exist in the brain of a patient with AD. These mice had higher Ab plaques and amyloid plaques, suggesting that BMDM is essential for Ab clearance.[20]
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