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Alzheimer's disease: how does it start?
1UCSD-Neuropathology Division, 1363 Shinly, Suite 100, Escondido, CA 92026, USA. jdelator@nctimes.net
Insights
Alzheimer's disease (AD) is a vascular disorder, not neurodegenerative. Reclassifying AD as vascular could improve treatment by targeting relevant pathology.
Area of Science:
- Neurology
- Pathology
- Epidemiology
Background:
- Alzheimer's disease (AD) is currently misclassified as a neurodegenerative disorder.
- When vascular lesions are present, AD is often categorized as vascular dementia.
- Compelling evidence suggests AD is fundamentally a vascular disorder with secondary neurodegenerative effects.
Purpose of the Study:
- To review evidence supporting the reclassification of Alzheimer's disease (AD) as a vascular disorder.
- To address inconsistencies in AD research and treatment stemming from its current classification.
- To propose new research directions for effective AD therapy.
Main Methods:
- Comprehensive review of interdisciplinary evidence (epidemiology, pharmacology, neuroimaging, clinical medicine, pathology, physiology, experimental research).
- Analysis of AD risk factors, clinical symptoms, and treatment outcomes in relation to vascular pathology.
- Examination of historical challenges in AD diagnosis and preclinical marker identification.
Main Results:
- Evidence from multiple disciplines supports AD as a vascular disorder.
- This perspective explains treatment failures, links to vascular risk factors, and similarities with vascular dementia.
- It also clarifies difficulties in preclinical neurodegenerative marker detection and paradoxical pathophysiological events.
Conclusions:
- Reclassifying AD as a vascular disorder is crucial for advancing treatment strategies.
- Focusing on relevant vascular pathology in clinical trials can improve therapeutic success.
- New research lines targeting vascular mechanisms offer potential for novel AD therapies.
Abstract:
Presently, non-genetic Alzheimer's disease (AD) is wrongly classified as a neurodegenerative disorder. When vascular lesions are present, AD is considered to be a vascular dementia. However, compelling evidence indicates that (AD) is a vascular disorder with neurodegenerative consequences. There is an urgent clinical need to ascertain the true cause of this dementia. In this review, evidence indicating that AD is a vascular disorder comes from a number of different disciplines including studies in epidemiology, pharmacology, neuroimaging, clinical medicine, pathology, physiology and experimental research. This collective evidence also addresses many previously puzzling questions regarding: i) past and present treatment failures in AD, ii) strange association of AD risk factors with many vascular-related disorders, iii) parallel lesions, clinical symptoms risk factors and potentially interchangeable treatments present in AD and vascular dementia, iv) historical difficulty in finding neurodegenerative markers to detect AD pre-clinically, and, v) paradoxical pathophysiologic events preceding AD neurodegenerative changes. Re-classifying AD as a vascular disorder would very likely improve the chances of finding a useful treatment for this disorder because clinical study designs could focus on more realistic and relevant pathologic targets than is presently practiced. A short summary of potential new research lines that may provide novel therapy in the treatment and management of AD is discussed.