Similarly, whereas one recent study found that PTSD did not increase risk of Aβ or tau burden using blood-based markers, another study found decreased plasma Aβ in World Trade Center responders with PTSD. By contrast, another study using PET imaging found that PTSD was indeed correlated with Aβ burden. Three recent positron emission tomography (PET) studies found that PTSD did not increase risk of Aβ or total tau (t-tau) burden. However, the results of human studies investigating the relationship between PTSD and AD biomarkers have been mixed. Preclinical studies have shown that stress accelerates Aβ and tau pathology through corticotropin-releasing factor (CRF) overproduction. The high prevalence of PTSD symptoms in populations such as military personnel underscores the need to understand the influence of PTSD symptoms on cognition in aging.Īlthough the mechanisms linking PTSD to Alzheimer’s disease (AD) and other dementias are unknown, there are several biological pathways that link stress with AD including neuroinflammation, metabolic disorders, and neuropathological markers such as beta-amyloid (Aβ) and tau. Studies have shown that patients with PTSD are twice as likely to develop dementia than those without PTSD, and a recent meta-analysis confirmed that PTSD is a strong risk factor for all-cause dementia. There is growing concern that PTSD confers elevated risk for mild cognitive impairment and dementia. PTSD has been linked with poorer performance on neurocognitive tasks across various domains including attention, working memory, processing speed, verbal learning and memory, and executive functions. ![]() Posttraumatic stress disorder (PTSD) is a chronic, debilitating condition characterized by symptoms including intrusive re-experiencing of a traumatic event, avoidance of reminders of the event, negative mood/cognitions, and hyperarousal.
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