A map of evidence using transcranial direct current stimulation (tDCS) to improve cognition in adults with traumatic brain injury (TBI).

Introduction: Cognition impairments often occur after a traumatic brain injury and occur at higher rates in military members. Cognitive symptoms impair daily function, including balance and life quality, years after the TBI. Current treatments to regain cognitive function after TBI, including medications and cognitive rehabilitation, have shown limited effectiveness. Transcranial direct current stimulation (tDCS) is a low-cost, non-invasive brain stimulation intervention that improves cognitive function in healthy adults and people with neuropsychologic diagnoses beyond current interventions. Despite the available evidence of the effectiveness of tDCS in improving cognition generally, only two small TBI trials have been conducted based on the most recent systematic review of tDCS effectiveness for cognition following neurological impairment. We found no tDCS studies that addressed TBI-related balance impairments. Methods: A scoping review using a peer-reviewed search of eight databases was completed in July 2022. Two assessors completed a multi-step review and completed data extraction on included studies using a priori items recommended in tDCS and TBI research guidelines. Results: A total of 399 results were reviewed for inclusion and 12 met the criteria and had data extracted from them by two assessors using Google Forms. Consensus on combined data results included a third assessor when needed. No studies using tDCS for cognition-related balance were found. Discussion: Guidelines and technology measures increase the identification of brain differences that alter tDCS effects on cognition. People with mild-severe and acute-chronic TBI tolerated and benefited from tDCS. TBI-related cognition is understudied, and systematic research that incorporates recommended data elements is needed to advance tDCS interventions to improve cognition after TBI weeks to years after injury.

E-cadherin deficiency promotes prostate macrophage inflammation and bladder overactivity in aged male mice.

Decreased E-cadherin immunostaining is frequently observed in benign prostatic hyperplasia (BPH) and was recently correlated with increased inflammation in aging prostate. Homozygous E-cadherin deletion in the murine prostate results in prostate inflammation and bladder overactivity at 6 months of age. However, this model is limited in that while E-cadherin is significantly reduced in BPH, it is not completely lost; BPH is also strongly associated with advanced age and is infrequent in young men. Here, we examined the functional consequences of aging in male mice with prostate luminal epithelial cell-specific E-cadherin heterozygosity. In control mice, aging alone resulted in an increase in prostate inflammation and changes in bladder voiding function indicative of bladder underactivity. At 24 months of age, mice with prostate-specific Cre-mediated heterozygous deletion of E-cadherin induced at 7 weeks of age developed additional prostatic defects, particularly increased macrophage inflammation and stromal proliferation, and bladder overactivity compared to age-matched control mice, which are similar to BPH/LUTS in that the phenotype is slow-progressing and age-dependent. These findings suggest that decreased E-cadherin may promote macrophage inflammation and fibrosis in the prostate and subsequent bladder overactivity in aging men, promoting the development and progression of BPH/LUTS.