Our previous data indicate that juvenile social play is masculinized by ER-mediated DA action in developing brain [15]; however, it remains to be determined if this is due to ER activity specifically within the BST and CeA.
Notably, increasing evidence indicates that BACE1 levels become elevated in AD brains as disease progresses; however, it remains unclear how the BACE1 upregulation may affect efficacies of therapeutic interventions including BACE1-inhibiting approaches.
However, it remains controversial in the brain networks, with arguments concerning the existence and emergence of the modular organization [62].
However, it remains controversial whether countercoup brain injury could be a significant risk factor for memory/processing speed impairments.
These differences are often interpreted as risk factors for the development of stuttering, however, it remains unclear whether differences in brain activity reflect neural substrates related to the cause of stuttering or plastic changes resulting from a lifetime of stuttering.
However, it remains unclear how and when the brain processes topological structures to guide future behaviour during everyday life.
However, it remains unclear whether there is a brain functional impairment in Chinese-speaking patients with schizophrenia.
However, it remains unknown whether resting-state spontaneous brain activity would differ as a function of MAOA genetic variation.
However, it remains unclear whether vitamin C directly influences brain pathology in AD patients and/or in animal models, as mouse is able to synthesize vitamin C endogenously.
However, it remains still unclear, whether these differences in brain activation are specific to number processing, or whether they belie more general cognitive processing deficits in subjects with Turner's-, fragile X-syndrome or brain injury.
