CMAJ • June 17, 2008; 178 (13). doi:10.1503/cmaj.1080053.
© 2008 Canadian Medical Association or its licensors
All editorial matter in CMAJ represents the opinions of the authors and not necessarily those of the Canadian Medical Association.
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Letters

Hypoxia and Alzheimer disease

Christopher Patterson, MD

Professor of Medicine, Division of Geriatric Medicine, McMaster University, Hamilton, Ont.

[One of the authors responds:]

My coauthors and I thank Sujoy Khan and Ioan Davies for their thoughtful response to our article.1 Before establishing a relationship between hypoxia and subsequent development of Alzheimer disease, one must consider 2 issues. The first is whether the cognitive changes observed during or after hypoxia are due to Alzheimer disease or other cognitive disorders. Recoverable cognitive dysfunction2 can persist for many months after hospital admissions and may simulate a dementia, although it is probably a type of subsyndromal delirium. The second is whether there are factors other than hypoxia (such as chronic inflammation3,4) that may account for cognitive changes. In addition to hypoxemia, tobacco smoking causes prolonged exposure to carbon monoxide, numerous carcinogens and other potential neurotoxins. Head injury not only produces localized hypoxemia but it may also influence the subsequent development of Alzheimer disease through the effects of hemorrhage, contusion and inflammatory responses. Both hypertension and tobacco smoking increase the risk of stroke, and the synergistic effect of Alzheimer disease and cerebrovascular disease is well known.5 In chronic obstructive lung disease, inflammatory cytokines,6 recurrent infections and conceivably the effects of anticholinergic medications could all contribute to the observed cognitive changes. Heart failure may also be associated with cognitive deficits, but many factors other than hypoxia, such as activation of neuroendocrine pathways, rheologic changes and consumption of numerous medications with known anticholinergic side effects, offer alternative explanations.7 Finally, the existence of anatomic changes pathognemonic of Alzheimer disease does not guarantee a phenotype of dementia.5

Khan and Davies raise an intriguing hypothesis, but our review cannot answer their question as we were limited by the methodologic constraints of longitudinal cohort studies, none of which consistently measured arterial oxygen tension or transcutaneous oxygen saturation levels. Only prospective studies will be able to answer their question.

Footnotes

Competing interests: None declared.


REFERENCES

  1. Patterson C, Feightner JW, Garcia A, et al. Diagnosis and treatment of dementia: 1. Risk assessment and primary prevention of Alzheimer disease. CMAJ 2008;178:548-56.[Abstract/Free Full Text]
  2. Inouye SK, Zhang Y, Han L, et al. Recoverable cognitive dysfunction at hospital admission in older persons during acute illness. J Gen Intern Med 2006;21:1276-81.[CrossRef][Medline]
  3. Heneka MT, O'Banion MK. Inflammatory processes in Alzheimer's disease. J Neuroimmunol 2007;184:69-91.[CrossRef][Medline]
  4. Mrak RE, Griffin WS. Glia and their cytokines in progression of neurodegeneration. Neurobiol Aging 2005;26:349-54.[CrossRef][Medline]
  5. Snowdon DA, Greiner LH, Mortimer JA, et al. Brain infarction and the clinical expression of Alzheimer disease. The Nun Study. JAMA 1997;277:813-7[Abstract/Free Full Text]
  6. Garrod R, Marshall J, Barley E, et al. The relationship between inflammatory markers and disability in chronic obstructive pulmonary disease (COPD). Prim Care Respir J 2007;16:236-40.[Medline]
  7. Heckman GA, Patterson CJ, Demers C, et al. Heart failure and cognitive impairment: challenges and opportunities. Clin Interv Aging 2007;2:209-18.[Medline]




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