DISTRIBUTION OF BETA-AMYLOID PROTEIN IN THE BRAIN FOLLOWING SEVERE HEAD-INJURY

被引：127

作者：

GRAHAM, DI

GENTLEMAN, SM

LYNCH, A

ROBERTS, GW

机构：

[1] CHARING CROSS & WESTMINSTER MED SCH,DEPT PSYCHIAT & ANAT,LONDON,ENGLAND

[2] SMITHKLINE BEECHAM PHARMACEUT,DEPT MOLEC NEUROPATHOL,HARLOW CM19 5AD,ESSEX,ENGLAND

来源：

NEUROPATHOLOGY AND APPLIED NEUROBIOLOGY | 1995年 / 21卷 / 01期

关键词：

BETA-AMYLOID PROTEIN; HEAD INJURY;

D O I：

10.1111/j.1365-2990.1995.tb01025.x

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

Deposits of beta-amyloid protein (beta AP) can be found in the brains of 30% of fatally head-injured patients; they have been found in children and after survival times of only 4 h. The principal aims of this study were to map the distribution of beta AP in 14 patients aged 65 years or less in whom it was known that the protein had been deposited, and to correlate its distribution with the pathologies of traumatic brain injury. The results show that beta AP is widely distributed, and that there is no correlation between its presence and cerebral contusions, intracranial haematoma, axonal injury, ischaemic brain damage, brain swelling or the pathology of raised intracranial pressure, These findings suggest that the deposition of beta AP is a consequence of the acute phase response of nerve cells to stress in susceptible individuals. Further studies will be required to establish the possible relationship between the deposition of beta AP following head injury and the molecular neuropathology of Alzheimer's disease.

引用

页码：27 / 34

页数：8

共 30 条

[11]

Gentleman SM, Bruton CJ, Allsop D., Lewis SJ, Polak JM, Roberts GW, A demonstration of the advantages of immunostaining in the quantification of amyloid plaque deposits, Histochemistry, 92, pp. 355-358, (1989)

[12]

Gentleman SM, Nash MJ, Sweetig CJ, Graham DI, Roberts GW, Beta amyloid precursor protein (β‐APP) as a marker for axonal injury after head injury, Neurosci Lett, 160, pp. 139-144, (1993)

[13]

Gentleman SM, Graham DI, Roberts GW, Molecular pathology of head trauma — altered β‐APP metabolism and the aetiology of Alzheimer's disease, Prog Brain Res, 96, pp. 237-246, (1993)

[14]

Gentleman SM, Roberts GW, Risk factors in Alzheimer's disease, Br Med J, 304, pp. 118-119, (1991)

[15]

Graham DI, Ford I., Adams JH, Et al., Ischaemic brain damage is still common in fatal non‐missile head injury, J Neurol Neurosurg Psyrhint, 52, pp. 346-350, (1989)

[16]

Grik WST, Sheng JG, Gentleman SM, Graham DI, ak RE, Roberts GW, Microglial interleukin‐1 expression in human head injury: correlations with neuronal and neuritic β‐amyloid precursor protein expression, Neurosci Lett, 176, pp. 133-136, (1994)

[17]

Huber A., Gabbert K., Kelemen J., Cervos-Navarro J., Density of amyloid plaques in brains after head trauma, J Neurotrauma, 10, (1993)

[18]

Kalaria RN, Perry G., Amyloid P component and other acute‐phase proteins associated with cerebellar Aβ‐deposits in Alzheimer's disease, Brain Res, 631, pp. 151-155, (1991)

[19]

Kawarabayashi T., Shoji M., Harigaya Y., Yamaguchi H., Hirai S., Expression of β‐APP in the early stage of brain damage, Brain Res, 563, pp. 334-338, (1991)

[20]

Mortimer JA, van Duijn CM, Chandra V., Head trauma as a risk factor for Alzheimer's disease: a collaborative re‐analysis of case control studies, International Journal of Epidemiology, 20, (1991)

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