Reduced cortical thickness in World Trade Center responders with cognitive impairment

Abstract

Introduction This study examined cortical thickness (CTX) in World Trade Center (WTC) responders with cognitive impairment (CI). Methods WTC responders (N = 99) with/without CI, recruited from an epidemiologic study, completed a T1‐MPRAGE protocol. CTX was automatically computed in 34 regions of interest. Region‐based and surface‐based morphometry examined CTX in CI versus unimpaired responders. CTX was automatically computed in 34 regions of interest. Region‐based measures were also compared to published norms. Results Participants were 55.8 (SD = 0.52) years old; 48 had CI. Compared to unimpaired responders, global mean CTX was reduced in CI and across 21/34 cortical subregions. Surface‐based analyses revealed reduced CTX across frontal, temporal, and parietal lobes when adjusting for multiple comparisons. Both CI and unimpaired WTC groups had reduced CTX in the entorhinal and temporal cortices compared to published normative data. Discussion Results from the first structural magnetic resonance imaging study in WTC responders identified reduced CTX consistent with a neurodegenerative disease of unknown etiology.

Pathway Analysis for Plasma β-Amyloid, Tau and Neurofilament Light (ATN) in World Trade Center Responders at Midlife

“…Finally, we measured plasma total tau as a marker for T and not plasma phospho-tau181. Whilst both have been demonstrated to effectively distinguish between AD and cognitively normal subjects in a clinical setting, pTau181 has been reported to be a more sensitive and specific predictor of elevated brain Ab and was associated with tau PET, whereas total tau was associated with cortical thickness in AD signature regions [45], which is an association that applies to our finding of reduced cortical thickness in the WTC responder population [46]. Therefore, future pathway analyses and considerations of the ATN model in AD pathogenesis should not only account for both subtypes of b-amyloid, but should also take into account both isoforms of plasma tau.…”

A Workshop on Cognitive Aging and Impairment in the 9/11-Exposed Population

“…Cognitive impairment was measured by clinicians using the MoCA. PTSD status, attained by trained psychologists using the Structured Clinical Interview for the Diagnostic and Statistical Manual of Mental Disorders-IV (SCID-IV) [ 105 ], did not predict reduced CTX across groups [ 106 ]. Both cognitively impaired and unimpaired groups had reduced CTX in the entorhinal and temporal cortices compared to published normative data.…”

“…There is emerging evidence that these regions are vulnerable to exposure to inhaled neurotoxins [ 107 ]. The authors noted that reduced CTX and volume of the entorhinal cortex is often interpreted as an early marker of the spread of tauopathy in AD [ 106 ]. Patterns of CTX reduction were most similar to those found in an uncommon parietal-dominant subtype of AD and related dementias.…”

Case Report: A World Trade Center (WTC) responder presenting with moderate stage dementia by age 57, suggesting an extended severity of WTC-associated illness'

“…Recent evidence indicates that World Trade Center Responders (WTCRs) are apparently at increased risk for a clinical syndrome that includes PTSD (post-traumatic stress disorder) and MCI (mild cognitive impairment) [1][2][3][4][5][6][7][8][9][10] . The association of these behavioral and cognitive symptoms was rst described by Bromet, Luft, Clouston, and colleagues [1][2][3] .…”

“…The association of these behavioral and cognitive symptoms was rst described by Bromet, Luft, Clouston, and colleagues [1][2][3] . No autopsy characterization of the syndrome has yet emerged, though bio uid and neuroimaging biomarker data support features of: (1) progressive behavioral and cognitive dysfunction, (2) proteinopathy involving the appearance of neurodegeneration-related molecules in the peripheral circulation, and (3) a substantial region loss of brain volume [4][5][6][7][8] . Inciting factors such as inhalation of neurotoxins and/or psychological stressors (or a combination of both) have been proposed as contributory to the pathogenesis, but no de nitive etiologic agent has been identi ed 8,9 .…”