Alzheimer's dementia and post-traumatic stress disorder; Differences and similarities in neuroimaging

Third Neurology Department, Aristotle University, Thessaloniki, Greece.
Hellenic journal of nuclear medicine (Impact Factor: 0.99). 11/2008; 12(1):41-6.
Source: PubMed


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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    • "Post-traumatic stress disorder (PTSD) is an anxiety disorder that may develop following exposure to a strongly or extremely traumatic event. Although PTSD is regarded as a long-term, maladaptive stress response in which the central nervous system is not directly affected [1–5], neuroimaging studies have demonstrated that some patients with PTSD show abnormally elevated activity and alterations in gray matter volume and density in the cortex, hippocampus, and corpus callosum [6–8]. The hippocampus and prefrontal cortex, receiving information from the multisensory system and higher cortex, are intrinsically related to learning and memory and play key roles in emotion and behavior. "
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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/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 · 1.43 Impact Factor
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    • "The hippocampus undergoes atrophy and contributes to the chronic memory deficits in the weeks to months following a mTBI (66, 67). Other studies reported that alterations in hippocampus ETC level is associated with aging and increased oxidative damage in mice brains (68) and with Alzheimer’s disease (69), a neurodegenerative disorder common among TBI patients (70, 71). "
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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
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    ABSTRACT: To explore the association between posttraumatic stress disorder (PTSD) and dementia in older veterans. Administrative database study of individuals seen within one regional division of the Veterans Affairs healthcare network. Veterans Integrated Service Network 16. Veterans aged 65 and older who had a diagnosis of PTSD or who were recipients of a Purple Heart (PH) and a comparison group of the same age with no PTSD diagnosis or PH were divided into four groups: those with PTSD and no PH (PTSD+/PH-, n=3,660), those with PH and no PTSD (PTSD-/PH+, n=1,503), those with PTSD and a PH (PTSD+/PH+, n=153), and those without PTSD or a PH (PTSD-/PH-, n=5,165). Incidence and prevalence of dementia after controlling for confounding factors in multivariate logistic regression. The PTSD+/PH- group had a significantly higher incidence and prevalence of dementia than the groups without PTSD with or without a PH. The prevalence and incidence of a dementia diagnosis remained two times as high in the PTSD+/PH- group as in the PTSD-/PH+ or PTSD-/PH- group after adjusting for the confounding factors. There were no statistically significant differences between the other groups. The incidence and prevalence of dementia is greater in veterans with PTSD. It is unclear whether this is due to a common risk factor underlying PTSD and dementia or to PTSD being a risk factor for dementia. Regardless, this study suggests that veterans with PTSD should be screened more closely for dementia. Because PTSD is so common in veterans, this association has important implications for veteran care.
    Journal of the American Geriatrics Society 09/2010; 58(9):1627-33. DOI:10.1111/j.1532-5415.2010.02977.x · 4.57 Impact Factor
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