All lights on Neuroinflammation Research Antibodies
The brain is considered a unique immune environment due to the blood brain barrier, however, some immune surveillance processes do occur within the meningeal spaces. In some instances, pro-inflammatory events in the CNS can be harmful to neurons.
Recent evidence suggests a CNS-specific lymphatic system connecting cerebrospinal fluid to deep cervical lymph nodes through cells that closely resemble lymphatic endothelial cells, indicating that the immune system plays a central role in neuronal repair.
A compromised blood brain barrier leads to infiltration of T cells into the CNS, releasing cytokines that contribute to neuronal inflammation by activating microglia, astrocytes, T cells and other immune cells. Chronic neuronal inflammation can lead to neuronal death and the release of toxic protein aggregates (Tau, β-amyloid and α-synuclein), accessory molecules (ApoE), and other cellular components leading to neurodegeneration and disease.
Recent research has shown that hyperphosphorylated, ubiquitinated, and N-terminally truncated TDP43 is the pathological hallmark lesion in most familial and sporadic forms of FTLD-U and ALS.
CX3CL1 is expressed by activated-endothelial cells, neurons, and astrocytes. The interaction of CX3CR1 and its ligand mediates cell firm adhesion and migration.
ApoE4 is a genetic variant of ApoE that is less effective at proteolytic degradation of amyloid β and is highly associated with increased Alzheimer's disease risk.