| 000 | 01873nam a2200253 4500 | ||
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| 001 | ESSALUD | ||
| 005 | 20260903101044.0 | ||
| 007 | ta | ||
| 008 | t pe ||||| |||| 00| 0 spa d | ||
| 040 | _aBMG | ||
| 041 | _aeng | ||
| 100 |
_aGreenberg, Steven M. _eAutor _954526 |
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| 245 | _aCerebral amyloid angiopathy | ||
| 300 | _apáginas: 1836-1845 | ||
| 520 | _aCerebral amyloid angiopathy is a major cause of hemorrhagic stroke, a frequent contributor to age-related cognitive impairment, and a key component in adverse responses to beta-amyloid (Aβ) immunotherapy. Defined by pathological deposition of Aβ in the small blood vessels of the brain, cerebral amyloid angiopathy is most often diagnosed on the basis of magnetic resonance imaging studies showing multiple hemorrhages or leptomeningeal blood products within or overlying the cerebral cortex. The disorder typically manifests as hemorrhagic stroke or as a contributing factor to cognitive decline and, less commonly, with transient focal neurologic symptoms or a cerebral inflammatory autoimmune syndrome. The high risk of recurrent hemorrhagic strokes associated with cerebral amyloid angiopathy poses a particular challenge in patients with indications for antithrombotic therapy and dictates a carefully individualized weighing of risks and benefits. Ongoing research is focused on tools to aid in risk prediction, early diagnostic markers, and identification of key pathogenic steps as targets for disease-modifying therapies. | ||
| 650 |
_aALERGIA _97055 |
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| 650 |
_aENFERMEDAD AUTOINMUNE _953665 |
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| 650 |
_aDEMENCIA _98165 |
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| 650 |
_aENFERMEDAD DE ALZHEIMER _95521 |
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| 650 |
_aGERIATRÍA _91852 |
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| 650 |
_aICTUS _954458 |
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| 773 | 0 |
_022717 _922676 _dMassachusetts NEJM Group _oNEJM015 _tThe New England Journal of Medicine _wESSALUD _x0028-4793 |
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| 942 |
_cARTICULOS _e2026-08-31 _zsqb |
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| 999 |
_c22919 _d22919 |
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