Table 2 BAMs in distinct neurological diseases

Alzheimer’s Disease

1. TgCRND8 transgenic mice

2. Tg2576 transgenic mice

1. PVM turnover reduce cerebral amyloid angiopathy

2. PVMs express both NOX2 and CD36, which exacerbate the Aβ-induced oxidative stress

3. PVMs promote the expression of C1QA, GRN, and CTSB in microglia, leading to aberrant phagocytosis of neuronal synapses

4. PVMs may express APOE4, which is associated with neurovascular alterations and BBB breakdown

[78, 114,115,116,117, 121, 123,124,125]

Parkinson’s Disease

1. α-Synuclein overexpression in transgenic mice

2. Human postmortem brain tissues

1. MHCII⁺ BAMs present antigens to CD4⁺ T cells to initiate the anti-α-synuclein CD4⁺ T cell response

2. The depletion of BAMs reduces microglia activation and the recruitment of Ly6C^hi monocytes and CD4⁺ Th cells

3. BAMs in the meninges may contribute to the clearance of brain α-synuclein via the glymphatic system and meningeal lymphatic vessels

4. CD68⁺ BAMs have been observed to interact with CD3⁺ T cells in human brain tissues

[79, 132, 133]

Ischemic Stroke

1. A rat model of ischemia–reperfusion

2. MCAO mouse model

3. Post-mortem brain tissues of patients

1. CD163⁺ BAMs enhance leukocyte recruitment and BBB permeability via the production of VEGF after ischemia

2. Proliferated CD163⁺ BAMs can migrate to the brain parenchyma and induce inflammation

3. After ischemia, CD206⁺CD169⁺ BAMs show proliferation in perivascular spaces and subsequently accumulate in the brain parenchyma

4. MHCII⁺ BAM subsets may promote neuroinflammation by regulating adaptive immune responses, cellular oxidative phosphorylation, endocytosis, and immune cell recruitment

[104, 141,142,143]

Multiple Sclerosis

1. Human samples

2. EAE mouse model

1. BAMs are associated with MS lesion types and correlate with the pathology of MS

2. A subset of BAMs expressing CD163, F13A1, and LYVE1 is involved in lesion inflammation and antigen presentation

3. Both sdΜΦ and PVMs in the leptomeninges participate in autoantigen presentation and the activation of autoreactive effector T cells

4. PVMs continue to proliferate during the chronic phase of MS

[80, 150, 151, 154, 157]

Brain Cancers

1. Mouse glioma model of GL261

2. Transgenic mouse with 4T1 mammary adenocarcinoma

3. Human brain metastasis tissues

4. Transgenic mouse models of lung and breast adenocarcinoma brain metastases

1. BAMs are evenly distributed in both naïve and glioma-bearing brains

2. LYVE1⁺MHCII^loCD206^hi PVMs are involved in the formation of a pre-metastatic niche around blood vessels during cancer metastasis

3. LYVE1⁺ PVMs may contribute to the breakdown of BBB during tumor metastasis to the brain

4. BAMs located in the meninges may play a role in facilitating cancer metastasis to brain-border structures

[44, 61, 171, 174, 176, 177]