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Objective: To examine the relationship between memory and basic physical mobility in an independent elderly population. Methods: We evaluated memory and physical mobility in 147 persons aged 60 years or older who were physically and cognitively independent. Memory was assessed by using the Rivermead Behavioral Memory Test (RBMT) and a total standardized profile score was used as an index of overall memory status. Additionally, we made a “score independent of walking ability” to exclude the effect of physical mobility on the RBMT score and a “score independent of prospective memory” to exclude the effect of executive function on the RBMT score. Basic physical mobility was assessed by using the Timed Up and Go test (TUG). The score was expressed as the time in seconds to perform the sequence of the action required in TUG. Results: The TUG score significantly correlated with the total standardized profile score (rs = −0.21, P

Background Several theories of cigarette craving suggest that dopaminergic function in the ventral striatum plays an important role. The objective of this study was to determine correlations between craving-related brain activation and dopamine D1 receptor (D1R) binding in smokers. Methods Twelve smokers and 12 nonsmoking controls underwent [ 15 O]H 2 O-positron emission tomography activation study and D1R-binding study using [ 11 C]SCH 23390, and the correlations between receptor binding and cue-induced regional cerebral blood flow (rCBF) changes were assessed. Consecutive D1R-binding changes were examined during a period of 6 months of postsmoking abstinence in five smokers. Results Cue-induced activation was observed in the left ventral striatum including the nucleus accumbens in smokers. D1R binding in the ventral striatum showed a negative relationship with cue-induced craving and rCBF changes. D1R binding was significantly low in smokers, and there was a trend of increase after smoking abstinence. Conclusions D1R binding and cue-induced rCBF changes in the ventral striatum suggest the important role of D1R in this region in cigarette craving.

To reveal the pathogenetic mechanism of post-traumatic stress disorder (PTSD), we modeled the ‘re-experience’ symptom of PTSD in healthy subjects, and investigated its neural substrates using PET activation experiments on an emotionally (fear) valenced episodic memory task and several contrast tasks. Ten right-handed healthy male volunteers underwent H215O-PET. Each subject was required to watch a horror film the previous day. During the PET scan, the subject was shown part of the film for 60 s immediately before the terrifying climax scene and told to recall the following scene. The subject did not watch the scene directly, but re-experienced fear induced by the trigger. The rCBF in this task compared with that in control tasks was analyzed with SPM99. The subjective emotional state of the subject in each task was evaluated using an analog scale. The main cerebral areas where rCBF significantly correlated with the task of emotionally valenced episodic memory, compared with the novel emotional task, were the left retrosplenial cortex (Brodmann's area: BA 31), the left visual association cortex (BA 19) and the right prefrontal cortex (BA 10). Although the retrosplenial cortex or the posterior cingulate gyrus has been regarded as engaged in processing either only emotion or only episodic memory, this area is considered to be involved in processing ‘emotionally valenced episodic memory’.

In patients with post-traumatic stress disorder (PTSD), re-experiencing the trauma is often induced by external cues in the environment. The cues, which were emotionally neutral for the patients before the traumatic event, become fearful ones after the event. This phenomenon is considered to be associated with fear conditioning. The paradigm was set up so that the emotionality changes in the patients with PTSD would be reproduced, and the regional cerebral blood flow (rCBF) measured with positron emission tomography (PET) was compared during exposure to the same stimuli before and after acquisition of fear conditioning. Ten healthy male subjects were asked to look at some emotionally neutral photos, then to watch a video with fearful content that also contained images similar to that presented in the photos, and afterwards to look at the photos again. Five of the 10 subjects felt that the object in the photos was more fearful after watching the video than before, and they were considered to have acquired fear conditioning. In those five subjects, the rCBF in the right amygdala and the left posterior cingulate gyrus after acquisition of fear conditioning significantly increased relative to the rCBF before conditioning. Thus, these regions seem to have a critical role in fear conditioning.

Background Peripheral benzodiazepine receptor (PBR) in the brain of Alzheimer's disease (AD) patients has been discussed in relation to the role of gliosis in AD. The PBR was shown to have the ability to reflect activated glial cells, including microglia. The role of activated microglia in AD is an important topic in the pathophysiology of AD. The aim of this study was to quantify PBR in AD brain with a new high-sensitive PBR ligand, [ 11 C]DAA1106. Methods Positron emission tomography (PET) scans with [ 11 C]DAA1106, a potent and selective ligand for PBR, were performed on 10 patients with AD and 10 age-matched control subjects. All patients had mild to moderate dementia. Duration of illness was 1–3 years at the time of the scans. The PBR binding in the regions of interest was quantified by binding potential (BP) obtained from compartmental model analysis with plasma input function. Results Mean BP was increased in the brain of AD patients compared with control subjects in all measured regions. Statistical significance reached across many of the regions examined, including dorsal and medial prefrontal cortex, lateral temporal cortex, parietal cortex, occipital cortex, anterior cingulate cortex, striatum, and cerebellum. Conclusions The broad increase of PBR binding measured with [ 11 C]DAA1106 in the brain of AD patients suggests a widespread existence of cellular reactions with PBR in relatively early-stage AD.

Memory functioning and its disorder are central to understanding posttraumatic stress disorder (PTSD). The intrusive recall of memories for the traumatic event, or reexperiencing, is a central feature of PTSD (Clark et al. 2003). In those suffering from this symptom, the past traumatic experience is recalled intrusively and without intent, including in nightmares, with a sense that the traumatic event is occurring right now, accompanied by emotional response such as fear, and physiological responses such as palpitation and dyspnea. Several neuroimaging studies with provocation of PTSD symptoms have been reported, in which reexperiencing was provoked using personalized trauma scripts or trauma-related sounds or pictures (Ranch et al. 1996; Shin et al. 1997, Bremner et al. 1999). These studies have suggested abnormalities in some brain regions such as the amygdala, Broca's area, and the anterior cingulate cortex (ACC) in patients with PTSD. However, few studies have investigated changes in neural activities during provocation of reexperiencing before and then after reported improvement of PTSD. We studied the neural basis of reexperiencing in patients with PTSD using positron emission tomography (PET) and investigated the change in the neural activities from before to after improvement of PTSD symptoms. As a therapy for PTSD, we used the eye movement desensitization and reprocessing (EMDR) procedure. Al