Alzheimer's disease as a capillary dementia.

In addition to the well known structural stigmata which accompany the senile dementia of Alzheimer, attention is called to the presence of a group of robust changes which affect the fine vessels (capillaries, capillary arterioles and capillary venules), particularly of the cerebral cortex. These alterations include irregular pouches and excrescences on the vessels (a "lumpy-bumby" appearance), general thickening of the basement membrane, loss of the fine perivascular neuronal plexus which seems to invest each vessel, no matter how small, and the appearance of pits or lacunae in the vessel walls of about one half of the Alzheimer patients studied. None of these changes have been seen in a group of approximately age-matched, non-demented controls. Much of this perivascular neural plexus originates within a few specific subcortical fields, especially the locus ceruleus and the nucleus basalis of Meynert and basal forebrain area. These also happen to be included among those brain areas which experience the most marked neuronal atrophy or loss in Alzheimer's disease. Since there is some evidence suggesting that surgically induced vascular denervation in myocardium produces dramatic changes in vascular wall structure we wonder whether neuronal pathology developing initially in these subcortical areas may not play a significant role in the development of the characteristic neuropathology in Alzheimer's disease. These speculations emphasize the possible importance of a failing blood brain barrier in the development of the disease.

[1]  J. Coyle,et al.  Alzheimer disease: Evidence for selective loss of cholinergic neurons in the nucleus basalis , 1981, Annals of neurology.

[2]  W. Bondareff,et al.  Loss of neurons of origin of the adrenergic projection to cerebral cortex (nucleus locus ceruleus) in senile dementia , 1982, Neurology.

[3]  T. Makinodan Immunobiology of Aging * , 1976, Journal of the American Geriatrics Society.

[4]  D. Ingvar,et al.  REGIONAL CEREBRAL BLOOD FLOW IN ORGANIC DEMENTIA WITH EARLY ONSET , 1970 .

[5]  B. K. Hartman,et al.  Central noradrenergic regulation of cerebral blood flow and vascular permeability. , 1975, Proceedings of the National Academy of Sciences of the United States of America.

[6]  D. Ingvar,et al.  Cognitive Reduction in Presenile Dementia Related to Regional Abnormalities of the Cerebral Blood Flow , 1976, British Journal of Psychiatry.

[7]  Ernst Scharrer,et al.  The Blood Vessels of the Nervous Tissue , 1944, The Quarterly Review of Biology.

[8]  K. Nandy Significance of brain-reactive antibodies in serum of aged mice. , 1975, Journal of Gerontology.

[9]  A. Brun Alzheimer’s Disease and its Clinical Implications , 1982 .

[10]  Y. Katayama,et al.  Long lasting suppression of firing of cortical neurons and decrease in cortical blood flow following train pulse stimulation of the locus coeruleus in the cat , 1981, Brain Research.

[11]  R. Delanoy,et al.  Locus coeruleus stimulation decreases deoxyglucose uptake in ipsilateral mouse cerebral cortex , 1979, Brain Research.

[12]  A. Scheibel,et al.  DENERVATION MICROANGIOPATHY IN SENILE DEMENTIA, ALZHEIMER TYPE , 1987, Alzheimer disease and associated disorders.

[13]  A. Scheibel,et al.  Progressive dendritic changes in aging human cortex , 1975, Experimental Neurology.