Technology and TBI: Perspectives of persons with TBI and their family caregivers on technology solutions to address health, wellness, and safety concerns.

Assistive technologies that are tailored to individuals' health, wellness, and safety concerns can help people with traumatic brain injury (TBI) and their family caregivers meet their goals. The purpose of this study was to investigate views of technology in the context of managing one's everyday life from the perspectives of persons with TBI and their family caregivers. We conducted 27 in-person, semi-structured interviews with persons with TBI (n = 15) and family caregivers (n = 12) and used conventional content analysis to analyze our data. The major themes that emerged were: 1) views of technology, 2) influence of technology on daily life, 3) desired technology solutions to address health, wellness, and safety concerns, and 4) barriers to adopting technology solutions. To address ongoing concerns, persons with TBI and family caregivers expressed a desire to have a patient portal to share information and communicate with providers, motion sensing devices to provide guidance for mobility, on-demand access to in-home rehabilitation therapy, access to a "social gym" where the persons with TBI could virtually exercise and interact with others, and technologies that help with sleep and facilitate peer support. These findings provide direction for implementation, design, or adaptation of technologies to address the concerns of this population.

Health, wellness, and safety concerns of persons with moderate-to-severe traumatic brain injury and their family caregivers: a qualitative content analysis.

BACKGROUND: Persons with moderate-to-severe traumatic brain injury (TBI) face issues with health, wellness, and safety that affect their ability to independently manage their care, even for individuals who are ≥75% independent in activities of daily living. These issues often lead to increased family involvement in managing the person's condition after discharge home. PURPOSE: We explored health, wellness, and safety concerns after discharge home from inpatient rehabilitation from the perspectives of persons with TBI who are ≥75% independent in activities of daily living and their family caregivers. MATERIALS AND METHODS: We interviewed 27 persons with TBI and family caregivers and used conventional content analysis to analyse the data. RESULTS: Seven themes related to health, wellness, and safety encompassed participants' experience. Health themes included: (1) attempting to manage medications and (2) navigating mental health difficulties. Wellness themes included: (1) working to stay physically active, (2) dealing with sleep and sleeplessness, and (3) adjusting to changing social relationships. Safety themes were: (1) addressing mobility challenges and (2) compensating for complications with cognitive functioning. CONCLUSIONS: Findings can guide the development of tools, supports, and resources to promote health, wellness, and safety of persons with TBI as they recover after discharge home.Implications for rehabilitationFindings on numerous concerns related to health, wellness, and safety suggest the need for implementation or development and testing of tools, supports, and resources to promote health, wellness, and safety of persons with traumatic brain injury as they recover after discharge home.Our findings can be used to educate healthcare providers and increase awareness of the nuanced challenges patients and families face after discharge home.Findings can also be used by providers to educate patients and families on realistic expectations for life after discharge.

DnaJA1 antagonizes constitutive Hsp70-mediated stabilization of tau.

Tau aggregation and amyloidogenesis are common hallmarks for neurodegenerative disorders called tauopathies. The molecular chaperone network constitutes the cellular defense against insults such as tau aggregation. However, chaperone effects on tau are dichotomous. Loss of tau's microtubule-binding activity facilitates an inappropriate chaperone interaction that promotes an amyloidogenic tau conformation. Conversely, other chaperones are capable of promoting tau clearance. Here, we demonstrate that a critical contributor to tau triage is the DnaJ-binding domain of Hsp70 proteins. In particular, over-expression of the constitutive DnaJ, DnaJA1, mediated tau clearance, while knockdown facilitated tau accumulation. This clearance was not specific to distinct pathogenic tau species. The activity of DnaJA1 was attenuated by concomitant increases in Hsp70. Tau reductions facilitated by DnaJA1 were dependent on the integrity of lysines known to be poly-ubiquitinated in human Alzheimer's brain. In vivo, DnaJA1 and tau levels were inversely correlated. The effects of DnaJA1 were partially specific: DnaJA1 reduced the levels of a polyQ protein but had no significant effect on α-synuclein levels. These data suggest that DnaJA1 triages all tau species for ubiquitin-dependent clearance mechanisms. Moreover, the levels of DnaJA1 and Hsp70 seem to play against each other with regard to tau: as DnaJA1 levels increase, tau levels are reduced, but this can be prevented if Hsp70 levels are simultaneously induced. Thus, the DnaJ repertoire possibly represents a powerful set of genetic modifiers for tau pathogenesis. Further investigations could provide new insights about triage decisions that facilitate or prevent amyloidogenesis of tau and other proteins associated with neurodegenerative disease.

Bending tau into shape: the emerging role of peptidyl-prolyl isomerases in tauopathies.

The Hsp90-associated cis-trans peptidyl-prolyl isomerase--FK506 binding protein 51 (FKBP51)--was recently found to co-localize with the microtubule (MT)-associated protein tau in neurons and physically interact with tau in brain tissues from humans who died from Alzheimer's disease (AD). Tau pathologically aggregates in neurons, a process that is closely linked with cognitive deficits in AD. Tau typically functions to stabilize and bundle MTs. Cellular events like calcium influx destabilize MTs, disengaging tau. This excess tau should be degraded, but sometimes it is stabilized and forms higher-order aggregates, a pathogenic hallmark of tauopathies. FKBP51 was also found to increase in forebrain neurons with age, further supporting a novel role for FKBP51 in tau processing. This, combined with compelling evidence that the prolyl isomerase Pin1 regulates tau stability and phosphorylation dynamics, suggests an emerging role for isomerization in tau pathogenesis.