Clusterin (9. Neural tissue)

Studies have demonstrated the overexpression of clusterin in various CNS disorders, such as certain gliomas, Alzheimer‘s disease and epilepsy, as well as after experimental brain injury in animals where different cell types were undergoing tissue remodelling or cell death ^Ref .

Clusterin is a ubiquitous multifunctional glycoprotein with the capability to interact with a broad spectrum of molecules, among them the Alzheimer‘s Abeta peptide. Due to its co-localization with fibrillar deposits in systemic and cerebral amyloid disorders, clusterin is also considered an amyloid-associated protein. Although no genuine function has been attributed to this protein so far, it has been implicated in a wide variety of physiological and pathological processes, a role that may vary according to the protein maturation, sub-cellular localization, and the presence of certain tissue- or cell-specific factors.

The abundance of clusterin RNA is increased in hippocampus from patients with Alzheimer disease and Pick disease ^Ref .

Ibotenic acid lesioning that caused death of striatal neurons also stimulated astrocytic responses as monitored by GFAP and clusterin ^Ref .

One clone was noticeably increased in retinitis pigmentosa in comparison with the control: partial sequencing showed it encoded clusterin ^Ref .

Adult male Wistar rats were subjected to 30 min of forebrain ischemia by four vessel occlusion. By 3 days after the ischemic insult, clusterin RNA levels were increased two fold in caudate nucleus and hippocampus. Clusterin protein levels assessed by immunoblots were markedly increased in both brain regions following ischemia. Glial fibrilary acidit protein (GFAP) RNA levels also increased over 5 fold in caudate nucleus and hippocampus following the ischemic insult. Despite significant elevations in GFAP RNA, protein levels of GFAP assessed by immunoblot were only marginally affected.the elevated expression of clusterin in rodent brain following this and other experimental lesion paradigms (e.g., excitotoxic lesions, deafferentation) suggest some general involvement of clusterin in neurodegeneration and remodelling following neuronal injury ^Ref .