Alzheimer's dementia and post-traumatic stress disorder differences and similarities in neuroimaging.
ABSTRACT There are studies supporting the suggestion that a severe psychological stress in the elderly can be the risk factor of Alzheimer's dementia (AB) and other types of dementia. We have reviewed the findings of single photon emission tomography, positron emission tomography, magnetic resonance imaging and functional magnetic resonance imaging (fMRI), related to brain function and structure in AD and in post traumatic stress disorder (PTSD). There is evidence that prefrontal and orbitofrontal cortices dysfunction contributes to PTSD symptomatology. Similarities between the two different aforementioned diseases exist in the areas of (a) medial temporal lobe, (b) hippocampus and (c) cingulated cortex.
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ABSTRACT: Background People who experience traumatic events have an increased risk of post-traumatic stress disorder (PTSD). However, PTSD-related pathological changes in the hippocampus and prefrontal cortex remain poorly understood. Material and Methods We investigated the effect of a PTSD-like animal model induced by severe stress. The experimental rats received 20 inescapable electric foot shocks in an enclosed box for a total of 6 times in 3 days. The physiological state (body weight and plasma corticosterone concentrations), emotion, cognitive behavior, brain morphology, apoptosis, and balance of gamma-aminobutyric acid (GABA) and glutamate in the hippocampus and prefrontal cortex were observed. Cell damages were examined with histological staining (HE, Nissl, and silver impregnation), while apoptosis was analyzed with flow cytometry using an Annexin V and propidium iodide (PI) binding and terminal deoxynucleotidyl transferase mediated-dUTP nick end labeling (TUNEL) method. Results In comparison with the sham litter-mates, the stressed rats showed decreased body weight, inhibition of hypothalamic-pituitary-adrenal (HPA) axis activation, increase in freezing response to trauma reminder, hypoactivity and anxiety-like behaviors in elevated plus maze and open field test, poor learning in Morris water maze, and shortened latency in hot-plate test. There were significant damages in the hippocampus but not in the prefrontal cortex. Imbalance between glutamate and GABA was more evident in the hippocampus than in the prefrontal cortex. Conclusions These results suggest that neuronal apoptosis in the hippocampus after severe traumatic stress is related to the imbalance between glutamate and GABA. Such modifications may resemble the profound changes observed in PTSD patients.Medical science monitor: international medical journal of experimental and clinical research 03/2014; 20:499-512. DOI:10.12659/MSM.890589 · 1.22 Impact Factor
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ABSTRACT: A significant proportion of the military personnel returning from Iraq and Afghanistan conflicts have suffered from both mild traumatic brain injury (mTBI) and post-traumatic stress disorder. The mechanisms are unknown. We used a rat model of repeated stress and mTBI to examine brain activity and behavioral function. Adult male Sprague-Dawley rats were divided into four groups: Naïve; 3 days repeated tail-shock stress; lateral fluid percussion mTBI; and repeated stress followed by mTBI (S-mTBI). Open field activity, sensorimotor responses, and acoustic startle responses (ASRs) were measured at various time points after mTBI. The protein expression of mitochondrial electron transport chain (ETC) complex subunits (CI-V) and pyruvate dehydrogenase (PDHE1α1) were determined in four brain regions at day 7-post mTBI. Compared to Naïves, repeated stress decreased horizontal activity; repeated stress and mTBI both decreased vertical activity; and the mTBI and S-mTBI groups were impaired in sensorimotor and ASRs. Repeated stress significantly increased CI, CII, and CIII protein levels in the prefrontal cortex (PFC), but decreased PDHE1α1 protein in the PFC and cerebellum, and decreased CIV protein in the hippocampus. The mTBI treatment decreased CV protein levels in the ipsilateral hippocampus. The S-mTBI treatment resulted in increased CII, CIII, CIV, and CV protein levels in the PFC, increased CI level in the cerebellum, and increased CIII and CV levels in the cerebral cortex, but decreased CI, CII, CIV, and PDHE1α1 protein levels in the hippocampus. Thus, repeated stress or mTBI alone differentially altered ETC expression in heterogeneous brain regions. Repeated stress followed by mTBI had synergistic effects on brain ETC expression, and resulted in more severe behavioral deficits. These results suggest that repeated stress could have contributed to the high incidence of long-term neurologic and neuropsychiatric morbidity in military personnel with or without mTBI.Frontiers in Neurology 12/2013; 4:196. DOI:10.3389/fneur.2013.00196
Article: Le vieillissement traumatique[Show abstract] [Hide abstract]
ABSTRACT: With the increase in life expectancy and dementia, the clinical question of post-traumatic stress disorder (PTSD) in the elderly is a major public health issue. PTSD is structured or restructured in old age according to several psychodynamic variants, which can be a reaction to a psychic trauma that is presented de novo; PTSD can also develop at a young age to later become chronic in old age. PTSD can thus be diagnosed very remotely, in time, from the event that was once the cause. The clinical presentation of PTSD is not constant but fluctuates over time: Following the apogee during the acute phase, the psychotraumatic symptoms decrease for a few years or even decades before increasing again at the start of old age. If traumatic or stressful life events that occur during old age can be isolated from a previously structured PTSD, the themes of the suffering experienced within the life history overlap. The symptoms of PTSD can evolve through absence, fluctuating over time to be updated in the elderly person through an organic pathology, sensory deficiency disorders, a cognitive decline or an institutionalization. Over time, the specific symptoms (reexperiencing, avoidance and hypervigilance) decrease in favor of nonspecific symptoms (asthenia, depression, use of psychoactive substances). The somatic presentation of PTSD is a fundamental aspect of the request for treatment in elderly patients: A somatic illness can lead to a PTSD de novo or cause old psychological psychotraumatic pain to reappear. With age the revivifications wane in favor of hypervigilance and avoidance strategies. The latter are at the forefront of “post-fall syndrome”, a syndrome considered as a psychotraumatic picture specific to the elderly person that develops into a normal aging process or dementia. In the face of a potentially traumatogenic situation, the integrity of the cognitive abilities is primordial to ensure a non-pathological psychological resolution. The difficulty in inhibiting traumatic memories will lead to their update. Likewise, PTSD is the locus of a decline in cognitive functions: recent or prolonged stress precedes the development of dementia in 80% of cases, playing the role of a triggering factor or facilitator. As revivifications are expressed more clinically due to neurocognitive disorders, it can be feared that the appearance or the exacerbation of a latent PTSD is the sign of the onset of dementia. Hypocampal atrophy with relative conservation of the amygdala is a biological support for dementia such as PTSD: pathological compensatory mnemic mechanisms could be at work here favoring productions that do not reflect real memories but thoughts guided by semantic knowledge. The absence of possibility of symbolizing death beyond life can fix thoughts on an ancient, unresolved confrontation where this death has already imposed itself. Far from a trivialization or a fatalistic vision of psychotraumatic disorders in elderly people, we wished to highlight research prospects, which open up the way to multidisciplinary questions notably including anthropological determinants. A dementia process can associate, at clinical level, hypo- and hypermnesic affections. It is thus fitting to assert the interest of considering dementia not only from a deficiency point of view but also according to its productive aspects. At an advanced stage of dementia it is difficult to establish a diagnosis of PTSD, all the more so as the emotional memory is affected.Annales Médico-psychologiques revue psychiatrique 01/2013; DOI:10.1016/j.amp.2012.04.007 · 0.15 Impact Factor