HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Correspondence: Submit a response Alert me when this article is cited Alert me when Correspondence are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Mehler, M. F. Articles by Dickson, D. W. Search for Related Content PubMed PubMed Citation Articles by Mehler, M. F. Articles by Dickson, D. W.

Reduced somatostatin-like immunoreactivity in cerebral cortex in nonfamilial dysphasic dementia

Departments of Pathology (Neuropathology) (Drs. Davies and Dickson) and Neurology (Dr. Mehler), Albert Einstein College of Medicine, Bronx, NY; and the Department of Pathology (Dr. Horoupian), Stanford University, Stanford, CA.

A nonfamilial syndrome is described in two middle-aged men who presented with progressive aphasia without incipient signs of cognitive impairment. In each case, 2 years elapsed before progressive functional decline or behavioral disabilities supervened. Radiologic studies documented asymmetric left cerebral atrophy that was progressive. The structure of the language disintegration was distinctive and not like that in Alzheimer's disease. Pathologic studies performed at postmortem examination of one patient documented asymmetric cerebral atrophy with nonspecific histopathologic changes. Biochemical studies revealed normal tissue levels of choline acetyltransferase activity, but reduced somatostatin-like immunoreactivity. Since cerebral somatostatin is largely present in intrinsic cortical neurons, while cholinergic innervation is largely derived from the basal forebrain, these findings suggest that nonfamilial dysphasic dementia may be an example of a distinct class of dementia due to intrinsic cortical degeneration, with sparing of the basal forebrain.

Address correspondence and reprint requests to Dr. Dickson, Department of Pathology (Neuropathology), Albert Einstein College of Medicine, K-438, 1300 Morris Park Avenue, Bronx, NY 10461.

Received November 10, 1986. Accepted for publication in final form December 30, 1986.

This article has been cited by other articles:

				M.-M. Mesulam Primary Progressive Aphasia -- A Language-Based Dementia N. Engl. J. Med., October 16, 2003; 349(16): 1535 - 1542. [Full Text] [PDF]

				Heterogeneity Among Alzheimer's Disease Patients J Geriatr Psychiatry Neurol, October 1, 1988; 1(4): 235 - 236. [PDF]