Brain infarction adds to the dementia
3-8 BRAIN INFARCTION AND THE CLINICAL EXPRESSION OF ALZHEIMER DISEASE: The Nun Study
"Significant numbers of individuals with abundant neuropathologic lesions of Alzheimer Disease (AD) do not become demented." The reason is not known. These investigators suspected that the clinical expression of AD may be partly determined by the presence of comorbid conditions such as brain infarcts. A significant number of individuals might develop dementia when both diseases co-exist. The combination might result in more severe dementia.
This study investigated the relationship between brain infarcts and cognitive function in a group of elderly women who had abundant senile plaques and some neurofibrillary tangles in the neocortex meeting the neuropathologic criteria for AD.
Conclusion: Cerebral vascular disease when combined with AD may play an important role in increasing dementia.

STUDY
1. Determined cognitive function and prevalence of dementia in nuns (n = 102; mean age 87) who later died. Identified brain infarcts at autopsy. Quantified senile plaques and neurofibrillary tangles in the frontal, temporal, and parietal lobes.

RESULTS

1. Of 102 participants, 61 met the neuropathological criteria for AD; 41 did not.
2. Among the 61 with neuropathologic criteria for AD, those with brain infarcts had poorer cognitive function and a higher prevalence of dementia (88%) than those without infarcts (57%).
3. Participants with lacunar infarcts in the basal ganglia, thalamus, or deep white matter had an especially high prevalence of dementia compared with those without such infarcts (odds ratio for dementia = 21). In this group fewer neuropathologic lesions of AD appeared to result in dementia.
4. Among the 41 participants who did not meet the neuropathologic criteria for AD, brain infarcts were only weakly associated with poor cognitive function and dementia.

DISCUSSION

1. In these women with pathological criteria for AD, concomitant brain infarcts were associated with poorer cognitive function and a higher prevalence of dementia.
2. Brain infarcts in participants who did not meet the pathological criteria for AD had only a weak association with dementia.
3. In this cohort about half of the participants had both AD and one or more infarcts, suggesting that the mixed form of dementia may be common in the elderly.
4. The relationship of brain infarcts to poor cognitive function appeared to be largely explained by lacunar infarcts in the basal ganglia, thalamus, and deep white matter. A few small infarcts in strategic regions of the brain made vulnerable by abundant neuropathological lesions of AD may be sufficient to produce dementia.
5. Cerebral atherosclerosis and the resulting brain infarcts may play a role in modifying the clinical expression of AD.

CONCLUSION
Cerebrovascular disease may play an important role in determining the presence and severity of the clinical symptoms of Alzheimer Disease.
JAMA March 12, 1997; 277: 813-17 Original investigation first author from Univ. Of Kentucky, Lexington

Comment:
Cerebral atherosclerosis and brain infarcts are largely preventable. We should protect our brains as well as our hearts. We can at least prevent part of the process. RTJ

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