This Article Full Text Full Text (PDF) All Versions of this Article: 37/12/2940    most recent 01.STR.0000248777.44128.93v1 Alert me when this article is cited Alert me if a correction is posted Citation Map 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 Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Aho, L. Articles by Alafuzoff, I. Search for Related Content PubMed PubMed Citation Articles by Aho, L. Articles by Alafuzoff, I. Pubmed/NCBI databases Gene GEO Profiles HomoloGene UniGene Genetics Home Reference Related Collections Ischemic biology - basic studies Other Research

(Stroke. 2006;37:2940.)
© 2006 American Heart Association, Inc.

Original Contributions

ß-Amyloid Aggregation in Human Brains With Cerebrovascular Lesions

From the Department of Clinical Medicine, Neurology (L.A., J.J.), and the Department of Clinical Medicine Neurology and Pathology (I.A.), Kuopio University, Finland.

Correspondence to Irina Alafuzoff, Kuopio University, P-O-B 1647, Harjulantie 1, Kuopio, Finland 70211. E-mail irina.alafuzoff{at}uku.fi

Background and Purpose— The present study assessed ß-amyloid (Aß) protein aggregates in postmortem human brains in subjects who had experienced stroke to examine the proposed association between ischemic stress and the accumulation of Aß reported in rodents.

Methods— A sample of 484 postmortem brains from nondemented subjects, lacking isocortical neurodegenerative pathology with verified cerebrovascular lesions, and 57 age-matched controls were assessed with respect to Aß, Aß40, and Aß42 aggregates in the cortex and thalamus by immunohistochemical techniques.

Results— The load of Aß aggregates did not display a significant association with cerebrovascular lesions. The load of Aß, Aß40, and Aß42 aggregates increased with age, and there was a tendency toward higher odds ratios for Aß aggregates, though not statistically significant, in subjects with acute cerebrovascular lesions. In the oldest subjects with cerebrovascular lesions and with both thalamic and cortical Aß aggregates, the load of thalamic Aß42 was significantly higher than the load of Aß40.

Conclusions— Our findings indicate that cerebrovascular disease does not influence the load of Aß, whereas a shift of aggregation from the Aß40 to the Aß42 residue is noted in the thalamus but only in aged subjects. It is impossible, however, to state whether this result is attributable to increased Aß production, its insufficient elimination, or other susceptibility factors.

Key Words: ß-amyloid • cerebrovascular lesions • human brain • immunohistochemistry • postmortem

This article has been cited by other articles:

				C. Justicia, P. Ramos-Cabrer, and M. Hoehn MRI Detection of Secondary Damage After Stroke: Chronic Iron Accumulation in the Thalamus of the Rat Brain Stroke, May 1, 2008; 39(5): 1541 - 1547. [Abstract] [Full Text] [PDF]