3D visualization of blood vessels in the Alzheimer’s disease mouse brain

Alzheimer’s disease (AD) is the most prevalent form of neurodegenerative disease that leads to profound cognitive decline in the elderly population. Despite decades of tremendous effort, we have not yet found effective therapeutic measurements to delay or prevent the progression of this devastating disease. Therefore, we need to find alternative approaches to conventional strategies such as clearing β-amyloid (Aβ) plaques or neurofibrillary tangles. Indeed, AD is a complex, multifactorial disease, and it is likely that various disease mechanisms contribute to pathology. One promising interdisciplinary approach is treatment of cerebrovascular dysfunction in AD patients. Increasing evidence suggests that cerebrovascular dysfunction is one of the pathological hallmarks of this disease. AD patients suffer from cerebral microinfarcts and a damaged cerebral vasculature, and a majority of patients with dementia present with both AD and vascular pathologies. Furthermore, some cerebrovascular symptoms such as white matter hyperintensity and carotid artery wave intensity start to increase 5 – 10 years prior to cognitive impairment onset. Circulatory deficiencies could therefore play an important role in AD progression, but the mechanism underlying the vascular contribution to AD is still unclear. Based on this idea, we are investigating the crosstalk between the cerebrovascular system and the nervous system to identify molecular targets and biomarkers underlying cerebrovascular deficits in AD.

X-ray crystallographic analysis shows that binding of Aβ42 alters fibrinogen (the main component of blood clots) structure

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