Authors named the later disease inflammatory macrophages and showed that, despite the high TREM2 expression, and contrarily to the neuroprotective DAMs, these macrophages expand in mice lacking TREM2, secrete TNF and might play a deleterious role by promoting a neuroinflammatory environment that further accelerates amyloid pathology and brain damage [153]. Here, TREM2 is linked to amyloidosis.