Altered basal forebrain BOLD signal variability at rest in posttraumatic stress disorder: A potential candidate vulnerability mechanism for neurodegeneration in PTSD.
Altered basal forebrain BOLD signal variability at rest in posttraumatic stress disorder: A potential candidate vulnerability mechanism for neurodegeneration in PTSD.
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DOI：
10.1002/hbm.25454
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发表时间：
2021-08-01
影响因子：
4.8
通讯作者：
Lanius RA
中科院分区：
文献类型：
--
作者：
Olivé I;Makris N;Densmore M;McKinnon MC;Lanius RA
Individuals with posttraumatic stress disorder (PTSD) are at increased risk for the development of various forms of dementia. Nevertheless, the neuropathological link between PTSD and neurodegeneration remains unclear. Degeneration of the human basal forebrain constitutes a pathological hallmark of neurodegenerative diseases, such as Alzheimer's and Parkinson's disease. In this seed‐based resting‐state (rs‐)fMRI study identifying as outcome measure the temporal BOLD signal fluctuation magnitude, a seed‐to‐voxel analyses assessed temporal correlations between the average BOLD signal within a bilateral whole basal forebrain region‐of‐interest and each whole‐brain voxel among individuals with PTSD (n = 65), its dissociative subtype (PTSD+DS) (n = 38) and healthy controls (n = 46). We found that compared both with the PTSD and healthy controls groups, the PTSD+DS group exhibited increased BOLD signal variability within two nuclei of the seed region, specifically in its extended amygdaloid region: the nucleus accumbens and the sublenticular extended amygdala. This finding is provocative, because it mimics staging models of neurodegenerative diseases reporting allocation of neuropathology in early disease stages circumscribed to the basal forebrain. Here, underlying candidate etiopathogenetic mechanisms are neurovascular uncoupling, decreased connectivity in local‐ and large‐scale neural networks, or disrupted mesolimbic dopaminergic circuitry, acting indirectly upon the basal forebrain cholinergic pathways. These abnormalities may underpin reward‐related deficits representing a putative link between persistent traumatic memory in PTSD and anterograde memory deficits in neurodegeneration. Observed alterations of the basal forebrain in the dissociative subtype of PTSD point towards the urgent need for further exploration of this region as a potential candidate vulnerability mechanism for neurodegeneration in PTSD. In this seed‐based resting‐state (rs‐)fMRI study we investigated the role of the human basal forebrain in PTSD, as a putative neuroimaging marker of PTSD‐related neurodegeneration. We observed an increased hemodynamic BOLD signal variability within the basal forebrain of PTSD subtype dissociative group, which mimics previous reports of dysfunction and degeneration of the basal forebrain in early phases of neurodegenerative diseases such as Alzheimer's disease. Observed alterations of the basal forebrain in the dissociative subtype of PTSD point toward the urgent need for further exploration of this region as a potential candidate vulnerability mechanism for neurodegeneration in PTSD.
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DOI：
10.3233/jpd-179001
发表时间：
2017
期刊：
Journal of Parkinson's disease
影响因子：
--
作者：
Braak H;Del Tredici K
通讯作者：
Del Tredici K
DOI：
10.1016/j.jalz.2017.04.014
发表时间：
2018-01
期刊：
Alzheimer's & dementia : the journal of the Alzheimer's Association
影响因子：
--
作者：
Flatt JD;Gilsanz P;Quesenberry CP Jr;Albers KB;Whitmer RA
通讯作者：
Whitmer RA
影响因子：
8.6
作者：
Carriere, Nicolas;Besson, Pierre;Devos, David
通讯作者：
Devos, David
影响因子：
3.8
作者：
DiLillo, David;Fortier, Michelle A.;Nash, Cindy
通讯作者：
Nash, Cindy
DOI：
10.1016/j.dadm.2019.01.003
发表时间：
2019-12-01
影响因子：
5.3
作者：
Clouston, Sean A. P.;Deri, Yael;Luft, Benjamin J.
通讯作者：
Luft, Benjamin J.