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Increasing evidence recognizes Alzheimer's disease (AD) as a multifactorial and heterogeneous disease with multiple contributors to its pathophysiology, including vascular dysfunction. The recently updated AD Research Framework put forth by the National Institute on Aging-Alzheimer's Association describes a biomarker-based pathologic definition of AD focused on amyloid, tau, and neuronal injury. In response to this article, here we first discussed evidence that vascular dysfunction is an important early event in AD pathophysiology. Next, we examined various imaging sequences that could be easily implemented to evaluate different types of vascular dysfunction associated

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The current development of immunotherapy for Alzheimer's disease is based on the assumption that human-derived amyloid ␤ protein (A␤) can be targeted in a similar manner to animal cell-derived or synthetic A␤. Because the structure of A␤ depends on its source and the presence of cofactors, it is of great interest to determine whether human-derived oligomeric A␤ species impair brain function and, if so, whether or not their disruptive effects can be prevented using antibodies. We report that untreated ex vivo human CSF that contains A␤ dimers rapidly inhibits hippocampal long-term potentiation in vivo and that acute systemic infusion of an anti-A␤ monoclonal antibody can prevent this disruption of synaptic plasticity. A␤ monomer isolated from human CSF did not affect long-term potentiation. These results strongly support a strategy of passive immunization against soluble A␤ oligomers in early Alzheimer's disease.

The VICCCS-2 suggests standardized use of the National Institute of Neurological Disorders-Canadian Stroke Network recommendations on neuropsychological and imaging assessment for diagnosis of VCI so as to promote research collaboration.