Feasibility study of a mobile application (ACT-ON) to complement acceptance and commitment therapy (ACT) intervention in cancer patients.

OBJECTIVE: Psychological and physical distress commonly affect cancer patients. Acceptance and commitment therapy (ACT) has shown promising results when it comes to ameliorating symptoms that may develop as a result of this. Meanwhile, it has come to light that the impact of psychological interventions may be enhanced by the use of mobile applications. However, to date no mobile applications have been developed to support ACT-based interventions in cancer patients. The aim of the present study is to develop and test the usability of a mobile application designed to complement face-to-face ACT-based therapy in a group of cancer patients undergoing treatment. MATERIALS AND METHODS: A total of thirty-nine patients were recruited to participate in this pilot study. Participants had to be: 18 years of age or over, currently undergoing treatment for breast, lung or colorectal cancer, in stage I-III, a smartphone user with daily internet access. The intervention sessions were administered for a period of eight weeks, one hour per week to groups of four to six participants. Patients had the ACT-ON mobile application at their disposal, which provided them with access to therapy-related activities: mindfulness, metaphors and exercises to clarify values. RESULTS: The application obtained adequate adoption (61.54%) and usage (54.17%) rates. Usability and ease of learning scores were as follows: good usability (M = 79.81, SD = 11.87); high usability (M = 80.53, SD = 14.04); ease of learning (M = 37.5, SD = 23.85). DISCUSSION: This is the first study to develop and evaluate the usability of an application designed to support ACT-based interventions in cancer patients undergoing treatment. The results show that the ACT-ON app is a feasible tool which achieves high levels of usability. However, said results ought to be confirmed by studies that include a larger number of cancer patients.

Identification of new molecular alterations in fatal familial insomnia.

Fatal familial insomnia is a rare disease caused by a D178N mutation in combination with methionine (Met) at codon 129 in the mutated allele of PRNP (D178N-129M haplotype). FFI is manifested by sleep disturbances with insomnia, autonomic disorders and spontaneous and evoked myoclonus, among other symptoms. This study describes new neuropathological and biochemical observations in a series of eight patients with FFI. The mediodorsal and anterior nuclei of the thalamus have severe neuronal loss and marked astrocytic gliosis in every case, whereas the entorhinal cortex is variably affected. Spongiform degeneration only occurs in the entorhinal cortex. Synaptic and fine granular proteinase K digestion (PrPres) immunoreactivity is found in the entorhinal cortex but not in the thalamus. Interleukin 6, interleukin 10 receptor alpha subunit, colony stimulating factor 3 receptor and toll-like receptor 7 mRNA expression increases in the thalamus in FFI. PrPc levels are significantly decreased in the thalamus, entorhinal cortex and cerebellum in FFI. This is accompanied by a particular PrPc and PrPres band profile. Altered PrP solubility consistent with significantly reduced PrP levels in the cytoplasmic fraction and increased PrP levels in the insoluble fraction are identified in FFI cases. Amyloid-like deposits are only seen in the entorhinal cortex. The RT-QuIC assay reveals that all the FFI samples of the entorhinal cortex are positive, whereas the thalamus is positive only in three cases and the cerebellum in two cases. The present findings unveil particular neuropathological and neuroinflammatory profiles in FFI and novel characteristics of natural prion protein in FFI, altered PrPres and Scrapie PrP (abnormal and pathogenic PrP) patterns and region-dependent putative capacity of PrP seeding.

Cannabinoid Receptor 2 Participates in Amyloid-ß Processing in a Mouse Model of Alzheimer's Disease but Plays a Minor Role in the Therapeutic Properties of a Cannabis-Based Medicine.

The endogenous cannabinoid system represents a promising therapeutic target to modify neurodegenerative pathways linked to Alzheimer's disease (AD). The aim of the present study was to evaluate the specific contribution of CB2 receptor to the progression of AD-like pathology and its role in the positive effect of a cannabis-based medicine (1:1 combination of Δ9-tetrahidrocannabinol and cannabidiol) previously demonstrated to be beneficial in the AßPP/PS1 transgenic model of the disease. A new mouse strain was generated by crossing AßPP/PS1 transgenic mice with CB2 knockout mice. Results show that lack of CB2 exacerbates cortical Aß deposition and increases the levels of soluble Aß40. However, CB2 receptor deficiency does not affect the viability of AßPP/PS1 mice, does not accelerate their memory impairment, does not modify tau hyperphosphorylation in dystrophic neurites associated to Aß plaques, and does not attenuate the positive cognitive effect induced by the cannabis-based medicine in these animals. These findings suggest a minor role for the CB2 receptor in the therapeutic effect of the cannabis-based medicine in AßPP/PS1 mice, but also constitute evidence of a link between CB2 receptor and Aß processing.