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D Dickson

Publications and source records attributed to D Dickson.

395 records · Page 22Linked to original sources
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Memory and mental status correlates of modified Braak staging.

We assessed the relationships of performance on memory and mental status tests and neuropathologic stage of Alzheimer's disease as defined by Braak and Braak in 29 patients from a prospective clinicopathologic series. We predicted that memory changes would occur at an earlier Braak stage than mental status changes. Staging was accomplished by matching the topographic distribution of neurofibrillary lesions detected with tau immunocytochemistry to the best fitting diagram published by Braak and Braak. Higher Braak stages were associated with decrements in performance on both memory and mental status tests. As predicted, memory performance declined from stages II to III and mental status did not decline until stages III to IV. The association between memory and Braak stage was unchanged after adjusting for neocortical senile plaques, whereas adjustments for Braak stage eliminated the association between cognitive functioning and amyloid burden. We conclude that Braak staging provides a useful summary of Alzheimer's disease neuropathology, which is associated with both memory and mental status performance.

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Familial Alzheimer's disease and cortical Lewy bodies: is there a genetic susceptibility factor?

The reason for the occurrence of Lewy body disease (LBD) in Alzheimer's disease (AD) patients is unknown. If brains from etiologically different AD groups differ in their tendency to develop cortical Lewy bodies, the concurrence of LBD in AD patients may be a manifestation of the AD process in specific AD subsets. To address this issue, we counted cortical Lewy bodies in AD patients with genetic abnormalities on chromosome 14 (n = 19), and chromosome 21 (n = 3), sporadic AD (n = 27), Down's syndrome (n = 1) and control (n = 26) patients. Cortical Lewy bodies were occasionally present in AD patients with long-duration disease in most of the above AD subgroups, but were not present in any of our age-matched control cases. We suggest that cortical Lewy body formation may be an intrinsic part of the late pathologic changes of AD regardless of etiology and that it is not specific to any of the AD subtypes studied.

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The significance of the extracellular matrix in intracranial aneurysms.

To what extent might change sin the extracellular matrix proteins in intracranial aneurysms (IA) or parent artery (PA) wall contribute to enlargement? Using IA specimens obtained from the coroner's office, the wall structure by light (Trichrome and Actin stains) and immunofluorescent microscopy (IF) (collagen I and fibronectin) have been studied in 18 specimens. It is well known that IA only arise when there is a deficiency in the internal elastic membrane and some breakdown in the media. The results show a normal three layer structure of intima, media, (muscularis), and adventitia in the PA extending out into the neck of the aneurysm. Immunofluorescent stains (IS) show collagen I and fibronectin limited to the adventitia and muscularis, respectively, of the PA and control arteries. The enlarging IA wall shows almost complete loss of this architecture. By IF stain, collagen I and fibronectin are intermingled throughout the IA wall. It is postulated that loss of structure and the confining muscularis layer permit easier elastic enlargement from a more or less homogeneous wall structure.

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