The Vietnam war has many legacies – including helping psychiatrists to better understand the nature of post-traumatic stress disorder (PTSD). Originally coined ‘the post-Vietnam syndrome’ there are now recognized DSM criteria that define PTSD more broadly and effectively.
Speaking at the APA in May 2016, Dr Alby Elias of the Mitcham Private Hospital in Melbourne, Australia said that some epidemiological studies suggest there is an increased risk of dementia – including Alzheimer’s disease (AD) – in people with PTSD. Furthermore, he said there have been neuroimaging studies in people with PTSD, reporting volume changes in hippocampal areas associated with cognition.
Dr Alby described how the psychological traumas of the Vietnam war have resulted in a veteran population with high lifetime- and point-prevalence of PTSD, with many veterans having persistent PTSD symptoms. Chronic PTSD is associated with cognitive impairments involving memory and attention. Dr Alby said that veterans with PTSD may report intrusive memories on the one hand and very impoverished memories and memory blackouts, on the other. He added that veterans with PTSD often report profound sensory changes affecting taste and smell perception.
These facts – the reports of dementia risk in PTSD and clear symptoms of cognitive impairment – have tempted speculation that PTSD might precede eventual AD, or share some of the neuropathological features of early AD.
Dr Alby said however that most studies to date which link PTSD and AD have been cross-sectional, often yielding conflicting results. He suggested this could in-part be due to the many potential confounding factors at play – such as the high rates of comorbidities in PTSD – including substance use disorder and co-occurrent psychiatric conditions like anxiety and depression which themselves can affect cognitive function. Dr Alby also pointed out that even prospective epidemiological studies in veterans reporting a significantly higher risk of dementia in people with PTSD, are problematic, since they fail to distinguish the type of dementia. He reminded the audience that the pathological processes underlying vascular dementia are very different from those of AD, for example.
Dr Alby said that many questions remain unanswered, such as – is PTSD associated with AD, or does it accelerate the processes leading to AD?
He reminded delegates of some core characteristics of AD and AD pathology. Neurofibrillary tangles, amyloid plaques and Tau proteins are associated with neurotoxicity in AD – with PET-visualized lesions a defining feature that correlates closely with the gold standard autopsy diagnosis of AD.
Dr Alby said that amyloid plaques and hypometabolism are detectible by PET scanning at least 5 years before symptoms of dementia emerge, and he suggested that 15-20 years before dementia, amyloid deposits can be detected by PET in patients who go on to develop AD. This, he said, suggests a pre-clinical or pre-AD phase in the progression and development of AD. Importantly, this pre-AD phase precedes the irreversible damage that comes to characterize AD.
Returning to the Vietnam veteran population with PTSD, Dr Alby said these military psychiatric patients offer an ideal group in which to study the potential links between PTSD and AD. He described his involvement in a neuroimaging study of Vietnam veterans from Australia and the US, which has looked at brain changes in subjects with PTSD as compared with control veterans. All subjects in the study had no evidence of dementia or AD. The objective was therefore to use neuroimaging to look for possible preclinical or pre-AD changes in brain neuropathology in subjects with PTSD.
Dr Alby said he was disappointed to report that the preliminary data from the neuroimaging study suggest there is no difference in amyloid burden or Tau retention, between veterans with PTSD and those without this diagnosis. He said that currently, this data therefore do not support previous reports of an increase in AD-like pathology in PTSD.
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