This review addresses an extremely important issue in the field of dementia research, that is, the fundamental contribution of vascular factors in the development of Alzheimer disease (AD), vascular dementia (VaD) and a mixture of the two, or so-called “mixed” dementia. According to Dr. Korczyn, mixed dementia is more common than either AD or VaD alone. This is not surprising because it is unusual to find a patient at autopsy who has been pathologically diagnosed with AD but shows no cerebrovascular lesions associated with ischemia or no cardiovascular abnormalities associated with cerebral hypoperfusion, or both conditions. This brings up the question as to whether AD or VaD can exist in “pure” form, that is, showing only pathologic changes that define either disorder. In our opinion, pure AD or VaD is rare or non-existent from a postmortem point of view and considerable pathologic findings in patients appear to support this conclusion. Dr. Korczyn also points out in his review that extensive pathologic changes characteristic of AD (plaques and tangles) may be present in the elderly brain at autopsy without demonstrable cognitive dysfunction at the time of death, thus questioning the necessity of such pathologic deposits as a requirement for AD to clinically “bloom.” Therefore, another question arises from this statement, namely, whether reduced cerebral blood flow as a consequence of a vascular risk factor (1) in an elderly individual simply “tips” the balance towards cognitive decline or is in fact the determining factor that triggers dementia in AD as it does in VaD. For that question to receive an adequate answer, clinical identification of the potential AD candidate must be available and reliable, for example, using screening techniques that can measure reduced cerebral blood flow (CBF) in normal elderly people (2) and then taking appropriate action to prevent further CBF deterioration by new treatments that can significantly alter the impending cognitive meldown. (3)
References:
Breteler MM.
Vascular risk factors for Alzheimer's disease: an epidemiologic perspective.
Neurobiol Aging. 2000 Mar-Apr;21(2):153-60.
PubMed.
Ruitenberg A, den Heijer T, Bakker SL, van Swieten JC, Koudstaal PJ, Hofman A, Breteler MM.
Cerebral hypoperfusion and clinical onset of dementia: the Rotterdam Study.
Ann Neurol. 2005 Jun;57(6):789-94.
PubMed.
de la Torre JC.
Is Alzheimer's disease a neurodegenerative or a vascular disorder? Data, dogma, and dialectics.
Lancet Neurol. 2004 Mar;3(3):184-90.
PubMed.
Comments
University of Texas at Austin
This review addresses an extremely important issue in the field of dementia research, that is, the fundamental contribution of vascular factors in the development of Alzheimer disease (AD), vascular dementia (VaD) and a mixture of the two, or so-called “mixed” dementia. According to Dr. Korczyn, mixed dementia is more common than either AD or VaD alone. This is not surprising because it is unusual to find a patient at autopsy who has been pathologically diagnosed with AD but shows no cerebrovascular lesions associated with ischemia or no cardiovascular abnormalities associated with cerebral hypoperfusion, or both conditions. This brings up the question as to whether AD or VaD can exist in “pure” form, that is, showing only pathologic changes that define either disorder. In our opinion, pure AD or VaD is rare or non-existent from a postmortem point of view and considerable pathologic findings in patients appear to support this conclusion. Dr. Korczyn also points out in his review that extensive pathologic changes characteristic of AD (plaques and tangles) may be present in the elderly brain at autopsy without demonstrable cognitive dysfunction at the time of death, thus questioning the necessity of such pathologic deposits as a requirement for AD to clinically “bloom.” Therefore, another question arises from this statement, namely, whether reduced cerebral blood flow as a consequence of a vascular risk factor (1) in an elderly individual simply “tips” the balance towards cognitive decline or is in fact the determining factor that triggers dementia in AD as it does in VaD. For that question to receive an adequate answer, clinical identification of the potential AD candidate must be available and reliable, for example, using screening techniques that can measure reduced cerebral blood flow (CBF) in normal elderly people (2) and then taking appropriate action to prevent further CBF deterioration by new treatments that can significantly alter the impending cognitive meldown. (3)
References:
Breteler MM. Vascular risk factors for Alzheimer's disease: an epidemiologic perspective. Neurobiol Aging. 2000 Mar-Apr;21(2):153-60. PubMed.
Ruitenberg A, den Heijer T, Bakker SL, van Swieten JC, Koudstaal PJ, Hofman A, Breteler MM. Cerebral hypoperfusion and clinical onset of dementia: the Rotterdam Study. Ann Neurol. 2005 Jun;57(6):789-94. PubMed.
de la Torre JC. Is Alzheimer's disease a neurodegenerative or a vascular disorder? Data, dogma, and dialectics. Lancet Neurol. 2004 Mar;3(3):184-90. PubMed.
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