2015
DOI: 10.1016/j.neubiorev.2015.05.008
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A critical review of chronic traumatic encephalopathy

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Cited by 99 publications
(69 citation statements)
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References 209 publications
(241 reference statements)
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“…The CSF results report normal value of CSF Aβ 1-42 protein, confirming the possibility that the cognitive decline associated with TBI could be triggered by a pathogenic mechanism different from the amyloidogenic cascade [8].…”
Section: Discussionsupporting
confidence: 57%
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“…The CSF results report normal value of CSF Aβ 1-42 protein, confirming the possibility that the cognitive decline associated with TBI could be triggered by a pathogenic mechanism different from the amyloidogenic cascade [8].…”
Section: Discussionsupporting
confidence: 57%
“…CSF T-tau and Aβ 1-42 were shown to optimally discriminate AD from other dementias in an autopsy-confirmed study [14]. On the contrary, amyloid beta deposition is not a pathologic feature of CTE [4], with the possibility to have normal beta amolyid value even in cases with severe cognitive decline (as in the case described here) [8]. Recent neuropathological studies of TBI cases have described amyloid plaques acutely after a single severe TBI and tau pathology after repeat TBI.…”
Section: Discussionmentioning
confidence: 50%
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“…6,43,54 While some reports support a causal link between neurocognitive decline and RBT, 64,65 others have suggested that the evidence is incomplete and that a direct causal link cannot be made at the present time. 11,26,27,62 Neuroimaging and neuropsychological testing represent evolving and commonly used modalities to quantify intracranial neurologic injury.…”
mentioning
confidence: 99%
“…For a comprehensive review of this literature see Manley et al [104], Iverson et al [111], Gardner et al [112], Randolph et al [113], and McCrory et al [114].…”
Section: Potential Longer Term Concernsmentioning
confidence: 99%