Abnormal blood clots and Alzheimer's disease

( therapeutic benefit for the treatment )

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Alzheimer's disease (AD) is a neurodegenerative disorder in which vascular pathology plays an important role. Since the β-amyloid peptide (Aβ) is a critical factor in this disease, we examined its relationship to fibrin clot formation in AD. In vitro and in vivo experiments showed that fibrin clots formed in the presence of Aβ are structurally abnormal and resistant to degradation. Fibrin(ogen) was observed in blood vessels positive for amyloid in mouse and human AD samples, and intravital brain imaging of clot formation and dissolution revealed abnormal thrombosis and fibrinolysis in AD mice. Moreover, depletion of fibrinogen lessened cerebral amyloid angiopathy pathology and reduced cognitive impairment in AD mice. These experiments suggest that one important contribution of Aβ to AD is via its effects on fibrin clots, implicating fibrin(ogen) as a potential critical factor in this disease.
The study, published by Cell Press in the June 10 issue of the journal Neuron, advances our understanding of the link between vascular pathology and AD and proposes a new therapeutic strategy aimed at slowing cognitive decline. One documented characteristic of AD is the deposition of β-amyloid peptide (Aβ) in the walls of cerebral blood vessels, known as cerebral amyloid angiopathy (CAA). CAA leads to a degeneration of blood vessel walls, compromised blood flow, and significant cognitive decline. There is also evidence that vascular diseases such as stroke, atherosclerosis, and hypertension are associated with an increased risk of dementia and AD, and that an abnormally elevated level of fibrinogen, the protein critical for blood clot formation, is correlated with AD. "Substantial evidence suggests that AD has a strong vascular component. However, there is no known mechanism that explains how Aβ could alter the process of blood clot formation," says senior study author, Dr. Sidney Strickland from the Laboratory of Neurobiology and Genetics at The Rockefeller University. Dr. Strickland and colleagues performed a series of experiments examining the relationship between Aβ and blood clot formation in AD.
They found that fibrin clots formed in the presence of Aβ were structurally abnormal and resistant to degradation. Importantly, AD mice with decreased levels of fibrinogen in their blood exhibited less Aβ accumulation in the walls of cerebral blood vessels and performed better in memory tasks. Based on these results, the authors propose a mechanism whereby the association between Aβ and fibrinogen causes altered blood clotting, leading to compromised blood flow and inflammation that contributes to the cognitive decline associated with AD. The authors go on to suggest that their proposed mechanism may be effectively targeted for treatment of AD. "A drug that could interfere with the effects of Aβ on fibrin clot formation would in theory normalize any blood clots formed in the brain, hence improving cerebral blood flow and neuronal function and survival," explains Dr. Strickland. "Because such a drug would have little effect on general clotting in other locations where Aβ levels are low, this approach could have significant therapeutic benefit for the treatment of AD." Read more: eurekalert.org(cell.com/neuron)

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