β-Amyloid Aggregation in Human Brains With Cerebrovascular Lesions

• Published in: Stroke (1970) Vol. 37; no. 12; pp. 2940 - 2945
• Main Authors: Aho, Leena, Jolkkonen, Jukka, Alafuzoff, Irina
• Format: Journal Article
• Language: English
• Published: Hagerstown, MD Lippincott Williams & Wilkins 01.12.2006
• Subjects: Adult; Aged; Aged, 80 and over; Amyloid beta-Peptides - analysis; Amyloid beta-Peptides - metabolism; Amyloidosis; Biological and medical sciences; Brain - pathology; Brain Chemistry; Cerebrovascular Disorders - metabolism; Cerebrovascular Disorders - pathology; Female; Humans; Investigative techniques, diagnostic techniques (general aspects); Male; Medical sciences; Metabolic diseases; Middle Aged; Nervous system; Neurology; Other metabolic disorders; Pathology; Patologi; Peptide Fragments - analysis; Peptide Fragments - metabolism; Retrospective Studies; Ultrasonic investigative techniques; Vascular diseases and vascular malformations of the nervous system; Human; Immunohistochemistry; Stroke; Nervous system diseases; Postmortem; Cardiovascular disease; Cerebral disorder; Vascular disease; human brain; Central nervous system disease; cerebrovascular lesions; Cerebrovascular disease; β-amyloid
• ISSN: 0039-2499; 1524-4628; 1524-4628
• DOI: 10.1161/01.STR.0000248777.44128.93

Background and Purpose— The present study assessed β-amyloid (Aβ) protein aggregates in postmortem human brains in subjects who had experienced stroke to examine the proposed association between ischemic stress and the accumulation of Aβ 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 Aβ, Aβ40, and Aβ42 aggregates in the cortex and thalamus by immunohistochemical techniques. Results— The load of Aβ aggregates did not display a significant association with cerebrovascular lesions. The load of Aβ, Aβ40, and Aβ42 aggregates increased with age, and there was a tendency toward higher odds ratios for Aβ aggregates, though not statistically significant, in subjects with acute cerebrovascular lesions. In the oldest subjects with cerebrovascular lesions and with both thalamic and cortical Aβ aggregates, the load of thalamic Aβ42 was significantly higher than the load of Aβ40. Conclusions— Our findings indicate that cerebrovascular disease does not influence the load of Aβ, whereas a shift of aggregation from the Aβ40 to the Aβ42 residue is noted in the thalamus but only in aged subjects. It is impossible, however, to state whether this result is attributable to increased Aβ production, its insufficient elimination, or other susceptibility factors.