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Overlap between pathology of Alzheimer disease and vascular dementia
1Department of Psychiatry, Institute for Health of the Elderly, Newcastle General Hospital, Newcastle upon Tyne, United Kingdom.
Insights
Alzheimer disease (AD) and vascular dementia (VaD) share significant neuropathological and genetic links, suggesting common therapeutic strategies may be effective for both conditions.
Area of Science:
- Neurology
- Pathology
- Genetics
Background:
- Alzheimer disease (AD) neuropathology extends beyond amyloid plaques and neurofibrillary tangles.
- Cerebrovascular pathology is present in over 30% of AD cases, with specific lesions evident in nearly all.
- Vascular dementia (VaD) patients often exhibit AD-type pathology, indicating overlapping disease mechanisms.
Purpose of the Study:
- To review cerebrovascular pathology in AD.
- To explore the link between peripheral vascular pathophysiology and dementia etiopathogenesis.
- To consider genetic influences, like apolipoprotein E, in the AD-VaD relationship.
Main Methods:
- Review of consortium data on AD neuropathology.
- Evaluation of cerebrovascular pathology in AD.
- Analysis of peripheral vascular pathophysiology in dementia.
- Consideration of genetic factors (e.g., apolipoprotein E) linking AD and VaD.
Main Results:
- Cerebrovascular lesions are common in AD, with some present in almost all cases.
- A significant portion of VaD cases show AD-type pathology.
- Shared pathological and genetic factors may link AD and VaD.
Conclusions:
- Cerebrovascular pathology plays a significant role in Alzheimer disease.
- The overlap between AD and VaD suggests common underlying mechanisms.
- Shared treatment strategies may be beneficial for both Alzheimer disease and vascular dementia.
Abstract:
There is overwhelming evidence to suggest that the neuropathology of Alzheimer disease (AD) extends beyond amyloid plaques and neurofibrillary tangles. Review of various consortium data shows that more than 30% of AD cases exhibit cerebrovascular pathology. However, certain vascular lesions such as cerebral amyloid angiopathy, microvascular degeneration, and periventricular white matter lesions are evident in almost all cases of AD. Whether these vascular lesions are coincidental or causal in the pathogenetic processes of AD remains to be defined. Although systemic vascular influences such as hypertension, coronary artery disease, and other cardiovascular disturbances may be responsible for such pathology in AD, it is equally intriguing that about one third of patients diagnosed with vascular dementia (VaD) will have AD-type pathology at autopsy. Moreover, previous studies have revealed that deficits in cholinergic indices related to the basal forebrain neurones are apparent in multi-infarct dementia. In this short review, we evaluate cerebrovascular pathology of AD in light of peripheral vascular pathophysiology implicated in the etiopathogenesis of the dementia. We also consider pathological findings in relation to genetic influences such as apolipoprotein E that may shed light on the link between AD and VaD. In view of these commonalties, it is reasonable to consider the same treatment strategies for both AD and VaD.