In the last decade, there has been a significant increase in the number of people diagnosed with dementia. With diminishing public health and social care resources, there is substantial need for assistive technology-based devices that support independent living. However, existing devices may not fully meet these needs due to fears and uncertainties about their use, educational support, and finances. Further challenges have been created by COVID-19 and the need for improved safety and security. We have performed a systematic review by exploring several databases describing assistive technologies for dementia and identifying relevant publications for this review. We found there is significant need for appropriate user testing of such devices and have highlighted certifying bodies for this purpose. Given the safety measures imposed by the COVID-19 pandemic, this review identifies the benefits and challenges of existing assistive technologies for people living with dementia and their caregivers. It also provides suggestions for future research in these areas.

Degenerate neural circuits perform the same function despite being structurally different. However, it is unclear whether neural circuits with interacting neuromodulator sources can themselves degenerate while maintaining the same neuromodulatory function. Here, we address this by computationally modeling the neural circuits of neuromodulators serotonin and dopamine, local glutamatergic and GABAergic interneurons, and their possible interactions, under reward/punishment-based conditioning tasks. The neural modeling is constrained by relevant experimental studies of the VTA or DRN system using, e.g., electrophysiology, optogenetics, and voltammetry. We first show that a single parsimonious, sparsely connected neural circuit model can recapitulate several separate experimental findings that indicated diverse, heterogeneous, distributed, and mixed DRNVTA neuronal signaling in reward and punishment tasks. The inability of this model to recapitulate all observed neuronal signaling suggests potentially multiple circuits acting in parallel. Then using computational simulations and dynamical systems analysis, we demonstrate that several different stable circuit architectures can produce the same observed network activity profile, hence demonstrating degeneracy. Due to the extensive D2-mediated connections in the investigated circuits, we simulate the D2 receptor agonist by increasing the connection strengths emanating from the VTA DA neurons. We found that the simulated D2 agonist can distinguish among sub-groups of the degenerate neural circuits based on substantial deviations in specific neural populations’ activities in reward and punishment conditions. This forms a testable model prediction using pharmacological means. Overall, this theoretical work suggests the plausibility of degeneracy within neuromodulator circuitry and has important implications for the stable and robust maintenance of neuromodulatory functions.