NIH conference. Alzheimer disease: clinical and biological heterogeneity.

R. P. Friedland, E. Koss, J. V. Haxby, C. L. Grady, J. Luxenberg, M. B. Schapiro, Jeffrey Kaye

Research output: Contribution to journalArticle

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Abstract

The clinical and biological features of Alzheimer disease are not uniform in their expression; heterogeneity is evident in the disease's clinical, anatomic, and physiologic characteristics. The presence of considerable intersubject and intrasubject heterogeneity suggests that subtypes of the disease exist. We define subtypes of Alzheimer disease in regard to the behavioral features (for example, predominant right or left hemisphere, or symmetrical impairment), inheritance (familial or sporadic), dosage of chromosome 21 (presence of the Down syndrome), time course of progression, age of onset (presenile or senile), and presence or absence of motor deficit (myoclonus or signs of an extrapyramidal syndrome). Studies of regional cerebral glucose metabolism with positron emission tomography and [18-fluorine] fluorodeoxyglucose show focal alterations in glucose use, with cerebral metabolic asymmetries in patients with Alzheimer disease that are related to the nature of the cognitive deficit. Serial roentgenographic computed tomographic studies show heterogeneous rates of lateral ventricle enlargement in the disease that are related to rates of cognitive decline. Similar anatomic and physiologic abnormalities are also found in persons 45 years of age or older who have the Down syndrome. Furthermore, patients with Alzheimer disease who have extrapyramidal dysfunction or myoclonus are a distinct subgroup, with specific abnormalities of central monoamine markers of dopamine metabolism, serotonin metabolism, and the hydroxylation cofactor, biopterin. The concept of subtypes in Alzheimer disease serves as a model with which the interactions of genetic influences with environmental factors can be examined.

Original languageEnglish (US)
Pages (from-to)298-311
Number of pages14
JournalAnnals of Internal Medicine
Volume109
Issue number4
StatePublished - Aug 15 1988
Externally publishedYes

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Alzheimer Disease
Myoclonus
Down Syndrome
Biopterin
Glucose
Chromosomes, Human, Pair 21
Lateral Ventricles
Fluorodeoxyglucose F18
Hydroxylation
Age of Onset
Positron-Emission Tomography
Dopamine
Serotonin

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Friedland, R. P., Koss, E., Haxby, J. V., Grady, C. L., Luxenberg, J., Schapiro, M. B., & Kaye, J. (1988). NIH conference. Alzheimer disease: clinical and biological heterogeneity. Annals of Internal Medicine, 109(4), 298-311.

NIH conference. Alzheimer disease : clinical and biological heterogeneity. / Friedland, R. P.; Koss, E.; Haxby, J. V.; Grady, C. L.; Luxenberg, J.; Schapiro, M. B.; Kaye, Jeffrey.

In: Annals of Internal Medicine, Vol. 109, No. 4, 15.08.1988, p. 298-311.

Research output: Contribution to journalArticle

Friedland, RP, Koss, E, Haxby, JV, Grady, CL, Luxenberg, J, Schapiro, MB & Kaye, J 1988, 'NIH conference. Alzheimer disease: clinical and biological heterogeneity.', Annals of Internal Medicine, vol. 109, no. 4, pp. 298-311.
Friedland RP, Koss E, Haxby JV, Grady CL, Luxenberg J, Schapiro MB et al. NIH conference. Alzheimer disease: clinical and biological heterogeneity. Annals of Internal Medicine. 1988 Aug 15;109(4):298-311.
Friedland, R. P. ; Koss, E. ; Haxby, J. V. ; Grady, C. L. ; Luxenberg, J. ; Schapiro, M. B. ; Kaye, Jeffrey. / NIH conference. Alzheimer disease : clinical and biological heterogeneity. In: Annals of Internal Medicine. 1988 ; Vol. 109, No. 4. pp. 298-311.
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