DIFFERENTIATING THE BEHAVIOURAL VARIANT OF ALZHEIMER’S DISEASE FROM BEHAVIOURAL VARIANT FRONTOTEMPORAL DEMENTIA AND TYPICAL ALZHEIMER’S DISEASE: THE VALUE OF NEUROIMAGING

Abstract

tion, Tomography Dementia Rating scale (TDR), MMSE, cerebral CT, MRI, SG, rheoencephalography (REG), cerebral MUGA. Test Group: 93 (8.24%) patients with AD. Control Group: 605 (53.59%) patients with mild and moderate level of chronic cerebrovascular insufficiency of atherosclerotic genesis, 342 (30.29%)with severe chronic cerebrovascular insufficiency, 27 (2.39%)with Binswanger’s disease, 62 (5.49%) with vascular parkinsonism. Results: All 93 (100%) Test Group patients showed specific CSVDs called dyscirculatory angiopathy of Alzheimer’s type (DAAT): absence of atherosclerotic changes of extra and intracerebral arteries; local decrease in the number of capillaries in the temporal and frontoparietal regions; local development of multiple arteriovenous shunts in the temporal and frontoparietal regions; local development of dilated venous trunks receiving blood from arteriovenous shunts of the temporal and frontoparietal regions; venous blood stagnation on the border of the frontal and parietal region; increased looping of distal intracerebral arteries. All 1036 (100%) Control Group patients demonstrated CSVD which were completely different from CSVD detected in patients with AD: 1004 (96.91%) patients had atherosclerotic changes of intracerebral arteries and arterioles; 932 (89.96%) areas of lowered capillary blood supply disseminated in different cerebral parts; 893 (86.20%) arteriovenous shunts disseminated in various cerebral parts-; no patients showed AD-specific local decrease in the number of capillaries, as well as no arteriovenous shunts in the temporal and frontoparietal parts; no AD-specific abnormally dilated venous trunks or blood stagnation at the level of the frontoparietal regions. Conclusions: CSVD with AD are manifested in dyscirculatory angiopathy of Alzheimer’s type (DAAT), which is characteristic only for AD. Similar changes in other neurodegenerative and ischemic diseases have been identified. DAAT is a specific etiological and pathogenetic sign of AD, the development of which leads to the deposition of amyloid beta in cerebral tissues and to AD appearance.