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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\u2010based resting\u2010state (rs\u2010)fMRI study identifying as outcome measure the temporal BOLD signal fluctuation magnitude, a seed\u2010to\u2010voxel analyses assessed temporal correlations between the average BOLD signal within a bilateral whole basal forebrain region\u2010of\u2010interest and each whole\u2010brain voxel among individuals with PTSD (<jats:italic>n<\/jats:italic>\u00a0=\u00a065), its dissociative subtype (PTSD+DS) (<jats:italic>n<\/jats:italic>\u00a0=\u00a038) and healthy controls (<jats:italic>n<\/jats:italic>\u00a0=\u00a046). 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\u2010 and large\u2010scale neural networks, or disrupted mesolimbic dopaminergic circuitry, acting indirectly upon the basal forebrain cholinergic pathways. These abnormalities may underpin reward\u2010related 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.<\/jats:p>","DOI":"10.1002\/hbm.25454","type":"journal-article","created":{"date-parts":[[2021,5,8]],"date-time":"2021-05-08T21:45:27Z","timestamp":1620510327000},"page":"3561-3575","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["Altered basal forebrain BOLD signal variability at rest in posttraumatic stress disorder: A potential candidate vulnerability mechanism for neurodegeneration in PTSD"],"prefix":"10.1002","volume":"42","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3843-398X","authenticated-orcid":false,"given":"Isadora","family":"Oliv\u00e9","sequence":"first","affiliation":[{"name":"Faculty of Brain Sciences, Division of Psychiatry University College of London  London United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nikos","family":"Makris","sequence":"additional","affiliation":[{"name":"Departments of Psychiatry and Neurology Services, Center for Neural Systems Investigation Center for Morphometric Analysis, Athinoula A. 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