Alzheimer’s is known to be a common form of dementia and a frequently recognized symptom is the incapability to recollect latest memories, such as inability to recall recently occurred events. The progression, severity and development of this disease have now been seemingly associated with a protein in the blood plasma known as clusterin.
Neuropathological alterations may be highlighted due to many findings in the blood and cerebrospinal fluid among Alzheimer patients. Cerebrospinal fluid has reduced levels of amyloid-beta peptides and augmented levels of total and phosphorylated tau concentration among individuals with the disease. These conditions underline the development of hallmark plaques and tangles in the blood. Previous analyses revealed that levels of specific metabolites and proteins in plasma may signify responses to brain modifications in Alzheimer’s disease, however none have been simulated.
Author’s share, “previous studies suggest that clusterin belongs to a family of extra cellular chaperones proteins that regulate the formation and removal of amyloid. Although these findings do not support the clinical utility of plasma clusterin concentration as a stand-alone biomarker for Alzheimer’s disease, they reveal a robust peripheral signature of this amyloid chaperone protein that is responsive to key features of disease pathology.”
In order to evaluate plasma proteins linked with Alzheimer’s disease, pathology experts adopted a combined proteomic and neuro-imaging method. Participants enlisted for the study included some with Alzheimer’s disease, while some with its precursor mild cognitive impairment whereas some did not have dementia. These participants underwent consistent clinical assessments and brain imaging scans. Further to highlight proteins linked with the disease the participants’ blood plasma was examined.
Authors elucidate, “Our findings clearly implicate clusterin, but there may well be other proteins in plasma related to the disease process, and indeed our previous studies and those of others suggest this is the case. These results may have wider implications for the identification of other amyloid chaperone proteins in plasma, both as putative Alzheimer’s disease biomarkers as well as drug targets of disease-modifying treatments.”
Experts identified that clusterin appeared to be lined with atrophy of the hippocampal region of the brain and with quick development of cognitive decline. Further they examined clusterin levels among 689 participants and revealed a connection between increased plasma levels of the protein and severity of disease. They also identified quick clinical formation and atrophy in the brain area known as entorhinal cortex that plays a significant role in memory. Augmented levels of clusterin in plasma were linked with having more amyloid-beta in the brain’s medial temporal lobe. Amyloid-beta forms the brain plaques linked with Alzheimer’s disease.
These findings are according to a report in the June issue of Archives of General Psychiatry.