Diabetics do not have increased Alzheimer-type pathology compared with age-matched control subjects - A retrospective postmortem immunocytochemical and histofluorescent study

被引:147
作者
Heitner, J
Dickson, D
机构
[1] ALBERT EINSTEIN COLL MED,DEPT PATHOL,BRONX,NY 10467
[2] ALBERT EINSTEIN COLL MED,DEPT NEUROL,BRONX,NY 10467
[3] ALBERT EINSTEIN COLL MED,RF KENNEDY CTR RES MENTAL RETARDAT & HUMAN DEV,BRONX,NY 10467
关键词
D O I
10.1212/WNL.49.5.1306
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Diabetics have impaired cognitive performance relative to age-matched control subjects, but the pathologic basis for this impairment is unknown. Because Alzheimer-type lesions, including both senile plaques and neurofibrillary tangles, contain glycated proteins and glycation is known to be increased in diabetes, we hypothesized that cognitive impairment in diabetes may be due in part to increased Alzheimer-type pathology. We measured the amount of Alzheimer-type pathology in postmortem brains of diabetics and age-matched control subjects with sensitive and specific histofluorescent and immunocytochemical methods. As expected, there were strong correlations between severity of senile plaques and neurofibrillary degeneration and age and also a strong correlation between the pathologic measures. On the other hand, there was no significant difference between diabetics and control subjects with respect to severity of Alzheimer-type pathology, on average, or with respect to age. This finding was true for diabetics with and without insulin dependence. The results confirm reports showing that diabetes is not a risk factor for Alzheimer-type pathology and suggest that factors other than Alzheimer's disease are responsible for cognitive impairment in diabetics.
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页码:1306 / 1311
页数:6
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共 44 条
  • [1] NEUROPATHOLOGICAL STAGING OF ALZHEIMER-RELATED CHANGES
    BRAAK, H
    BRAAK, E
    [J]. ACTA NEUROPATHOLOGICA, 1991, 82 (04) : 239 - 259
  • [2] Braak H, 1993, ALZHEIMERS DIS ADV C, P131
  • [3] GLYCATION PRODUCTS AND THE PATHOGENESIS OF DIABETIC COMPLICATIONS
    BROWNLEE, M
    [J]. DIABETES CARE, 1992, 15 (12) : 1835 - 1843
  • [4] BROWNLEE M, 1988, NEW ENGL J MED, V318, P1315
  • [5] GENE DOSE OF APOLIPOPROTEIN-E TYPE-4 ALLELE AND THE RISK OF ALZHEIMERS-DISEASE IN LATE-ONSET FAMILIES
    CORDER, EH
    SAUNDERS, AM
    STRITTMATTER, WJ
    SCHMECHEL, DE
    GASKELL, PC
    SMALL, GW
    ROSES, AD
    HAINES, JL
    PERICAKVANCE, MA
    [J]. SCIENCE, 1993, 261 (5123) : 921 - 923
  • [6] Curb J. D., 1996, Neurobiology of Aging, V17, pS122, DOI 10.1016/S0197-4580(96)80490-8
  • [7] Dickson DW, 1996, NEUROBIOL AGING, V17, P733
  • [8] DICKSON DW, 1995, RESEARCH ADVANCES IN ALZHEIMER'S DISEASE AND RELATED DISORDERS, P371
  • [9] The pathogenesis of senile plaques
    Dickson, DW
    [J]. JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY, 1997, 56 (04) : 321 - 339
  • [10] DICKSON DW, 1992, NEUROBIOL AGING, V13, P1