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The year 2011 will be pivotal for research and care of patients with Alzheimer disease (AD). The 27-year-old diagnostic criteria1 that have defined AD as diagnosis of exclusion have undergone revision. Key features of these criteria include the use of biomarkers to support a diagnosis of AD. In particular, these biomarkers include both CSF and PET measures of β-amyloid (Aβ) pathology. While there is still considerable uncertainty about the factors responsible for the initiation and progression of AD, the use of in vivo measures of Aβ pathology has undoubtedly revolutionized research and will soon affect clinical diagnosis.
One of the most problematic diagnostic questions has involved the interaction between AD and vascular pathology. For years clinicians have had access to imaging techniques such as CT and MRI that permit the evaluation of ischemic lesions. This has led to imaging-based criteria for vascular dementia. However, without an in vivo marker of Aβ pathology, understanding the contribution of AD pathology to persons diagnosed with vascular etiologies has largely relied upon autopsy. Many autopsy studies indicated that isolated subcortical vascular pathology is a relatively uncommon cause of dementia, with most such cases having moderate to severe plaque and tangle pathology as well.2 However, these autopsy studies are limited since they may …
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