Background: The mild cognitive impairment (MCI) stage among elderly individuals is very complex, and the level of diagnostic accuracy is far from ideal. Some studies have tried to improve the 'MCI due to Alzheimer's disease (AD)' classification by further stratifying these patients into subgroups. Depression-related symptoms may play an important role in helping to better define the MCI stage in elderly individuals.
Objective: In this work, we explored functional and structural differences in the brains of patients with nondepressed MCI (nDMCI) and patients with MCI with depressive symptoms (DMCI), and we examined how these groups relate to AD atrophy patterns and cognitive functioning.
Methods: Sixty-five participants underwent MRI exams and were divided into four groups: cognitively normal, nDMCI, DMCI, and AD. We compared the regional brain volumes, cortical thickness, and white matter microstructure measures using diffusion tensor imaging among groups. Additionally, we evaluated changes in functional connectivity using fMRI data.
Results: In comparison to the nDMCI group, the DMCI patients had more pronounced atrophy in the hippocampus and amygdala. Additionally, DMCI patients had asymmetric damage in the limbic-frontal white matter connection. Furthermore, two medial posterior regions, the isthmus of cingulate gyrus and especially the lingual gyrus, had high importance in the structural and functional differentiation between the two groups.
Conclusion: It is possible to differentiate nDMCI from DMCI patients using MRI techniques, which may contribute to a better characterization of subtypes of the MCI stage.
Drug addiction or substance use disorder (SUD), has been conceptualized as a three-stage (i.e. binge/intoxication, withdrawal/negative affect, and preoccupation/anticipation/craving) recurring cycle that involves complex changes in neuroplasticity, reward, motivation, desire, stress, memory, and cognitive control, and other related brain regions and brain circuits. Neuroimaging approaches, including magnetic resonance imaging, have been key to mapping neurobiological changes correlated to complex brain regions of SUD. In this review, we highlight the neurobiological mechanisms of these three stages of addiction. The abnormal activity of the ventral tegmental, nucleus accumbens, and caudate nucleus in the binge/intoxication stage involve the reward circuit of the midbrain limbic system. The changes in the orbitofrontal cortex, dorsolateral prefrontal cortex, amygdala, and hypothalamus emotional system in the withdrawal/negative affect stage involve increases in negative emotional states, dysphoric-like effects, and stress-like responses. The dysregulation of the insula and prefrontal lobes is associated with craving in the anticipation stage. Then, we review the present treatments of SUD based on these neuroimaging findings. Finally, we conclude that SUD is a chronically relapsing disorder with complex neurobiological mechanisms and multimodal stages, of which the craving stage with high relapse rate may be the key element in treatment efficacy of SUD. Precise interventions targeting different stages of SUD and characteristics of individuals might serve as a potential therapeutic strategy for SUD.
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