Targeting neurodegeneration to prevent post-traumatic epilepsy

被引：25

作者：

Ali, Idrish ^{[1
,2
]}

Silva, Juliana C. ^{[1
,2
]}

Liu, Shijie ^{[1
,2
]}

Shultz, Sandy R. ^{[1
,2
]}

Kwan, Patrick ^{[1
,2
]}

Jones, Nigel C. ^{[1
,2
]}

O'Brien, Terence J. ^{[1
,2
]}

机构：

[1] Monash Univ, Alfred Hosp, Cent Clin Sch, Dept Neurosci, Melbourne, Vic, Australia

[2] Univ Melbourne, Royal Melbourne Hosp, Dept Med, Melbourne, Vic, Australia

来源：

NEUROBIOLOGY OF DISEASE | 2019年 / 123卷

关键词：

Neurodegeneration; Tauopathies; beta amyloid; Neuroinflammation; Traumatic brain injury; Post-traumatic epilepsy; TRAUMATIC BRAIN-INJURY; AMYLOID PRECURSOR PROTEIN; MICROTUBULE-ASSOCIATED PROTEIN-2; CEREBROSPINAL-FLUID BIOMARKERS; MILD COGNITIVE IMPAIRMENT; TAU TRANSGENIC MICE; ALZHEIMERS-DISEASE; SODIUM SELENATE; MOUSE MODEL; STATUS EPILEPTICUS;

D O I：

10.1016/j.nbd.2018.08.006

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

In the quest for developing new therapeutic targets for post-traumatic epilepsies (PTE), identifying mechanisms relevant to development and progression of disease is critical. A growing body of literature suggests involvement of neurodegenerative mechanisms in the pathophysiology of acquired epilepsies, including following traumatic brain injury (TBI). In this review, we discuss the potential of some of these mechanisms to be targets for the development of a therapy against PTE.

引用

页码：100 / 109

页数：10

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