scholarly journals Zoo Therapy for Alzheimer’s Disease with Real-Time Speech Instruction and Neurofeedback System

2021 ◽  
Author(s):  
Yan Ai ◽  
Hamdi Ben Abdessalem ◽  
Claude Frasson
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Virtual Reality ◽  
Real Time ◽  
Positive Impact ◽  
Negative Emotions ◽  
Animal Therapy ◽  
Preliminary Results ◽  
Emotional Value ◽  
The Impact

There is an increasing number of people with Alzheimer’s disease. Negative emotions are not only one of the symptoms of AD, but also the accelerator of the disease. Animal therapy can have a positive impact on the negative emotions of patients, but it has strict requirements for both environments and animals. In this study, we aim to explore the effectiveness of using virtual animals and their impact on the reduction of patients’ negative emotions to improve the user’s cognitive functions. This approach has been implemented in the Zoo Therapy project, which presents an immersive 3D virtual reality animal environment, where the impact on the patient’s emotion is measured in real-time by using electroencephalography (EEG). In addition to creating highly realistic virtual animals, the innovation of Zoo Therapy is also in its communication mechanism as it implements bidirectional human-computer interaction supported by 3 interaction methods: 3D buttons, speech instruction, and Neurofeedback. Patients can actively interact with virtual animals through 3D buttons or speech instructions. The Neurofeedback system will guide the animal to actively interact with the patients according to their real-time emotional changes to reduce their negative emotions. Experiments and preliminary results show that it is possible to interact with virtual animals in Zoo Therapy, and the Neurofeedback system can intervene in Zoo VR environment when the emotional value goes down and might reduce patients’ negative emotions.

Potentially modifiable factors associated with agitation and aggression in Alzheimer’s disease: results of the ICTUS study

2019 ◽  
Vol 31 (10) ◽  
pp. 1509-1516 ◽  
Author(s):  
Adelaide de Mauleon ◽  
Maria Soto ◽  
Pierre Jean Ousset ◽  
Fati Nourhashemi ◽  
Benoit Lepage ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Affective Disorder ◽  
Positive Impact ◽  
Neuropsychiatric Symptoms ◽  
Cognitive Status ◽  
Community Dwelling ◽  
Factors Associated ◽  
Modifiable Factors ◽  
The Impact

ABSTRACTObjectives:To study potentially modifiable factors associated with the severity of agitation or aggression (A/A) symptoms among Alzheimer’s disease (AD) patients.Design:Data from the Impact of Cholinergic Treatment Use (ICTUS) study, European longitudinal prospective observational study.Setting:Community dwelling outpatients included in 29 European memory clinics.Participants:1375 participants with probable AD (Mini-Mental State Examination score of 10–26) with an informal caregiver.Measurements:At baseline and twice yearly over the two-year follow-up, patients underwent comprehensive clinical and neuropsychological assessments: sociodemographic data, cognitive status, functional impairment, and assessment of neuropsychiatric symptoms based on Neuro-Psychiatric Inventory (NPI). The ZARIT scale assessed the caregiver’s burden. The variable of interest was the severity of the item of A/A of the NPI. To study factors associated to the severity of A/A symptoms six months later, a multivariate mixed regression model was used.Results:Frequency of A/A symptom varied from 30% to 34% at each visit. Two factors were found to be independently associated with the severity of A/A: (1) the presence of affective disorder (anxiety, depression, and/or irritability) that increased the severity of the A/A by 0.89 point (coefficient:0.89; 95% Confidence Interval (CI) = [0.48,1.30], p < 0.001), and (2) a severe caregiver burden that increased the severity of the A/A by 1.08 point (coefficient:1.08; 95% CI = [0.69,1.47], p < 0.001).Conclusion:Research should evaluate whether the identification and treatment of an affective disorder along with the evaluation and optimal management of the caregiver would have a positive impact on the course of A/A in mild to moderate AD patients.

scholarly journals Virtual reality and real-time neurofeedback functional MRI: a breakthrough in foreseeing Alzheimer’s disease?

Brain ◽  
2020 ◽  
Vol 143 (3) ◽  
pp. 722-726 ◽  
Author(s):  
Federica Agosta ◽  
Elisa Canu ◽  
Massimo Filippi
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Virtual Reality ◽  
Real Time ◽  
Functional Mri ◽  
Closed Loop

This scientific commentary refers to ‘Earliest amyloid and tau deposition modulate the influence of limbic networks during closed-loop hippocampal downregulation’ by Skouras etal. (doi:10.1093/brain/awaa011).

Virtual Reality Orientation Game for Alzheimer’s Disease Using Real-Time Help System

2020 ◽  
pp. 13-23
Author(s):  
Manish Kumar Jha ◽  
Hamdi Ben Abdessalem ◽  
Marwa Boukadida ◽  
Alexie Byrns ◽  
Marc Cuesta ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Virtual Reality ◽  
Real Time ◽  
Reality Orientation ◽  
Help System

scholarly journals Cinnamaldehyde Improves Lifespan and Healthspan in Drosophila melanogaster Models for Alzheimer’s Disease

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Hanh M. Pham ◽  
Anna Xu ◽  
Samuel E. Schriner ◽  
Evgueni A. Sevrioukov ◽  
Mahtab Jafari
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Drosophila Melanogaster ◽  
Short Term Memory ◽  
Positive Impact ◽  
Fruit Fly ◽  
Cinnamon Extract ◽  
Positive Effects ◽  
Climbing Ability ◽  
The Impact

Cinnamon extract has been reported to have positive effects in fruit fly and mouse models for Alzheimer’s disease (AD). However, cinnamon contains numerous potential active compounds that have not been individually evaluated. The main objective of this study was to evaluate the impact of cinnamaldehyde, a known putative active compound in cinnamon, on the lifespan and healthspan of Drosophila melanogaster models for Alzheimer’s disease, which overexpress Aβ42 and MAPT (Tau). We found that cinnamaldehyde significantly improved the lifespan of both AD and non-AD flies. Cinnamaldehyde also improved the healthspan of AD flies overexpressing the Tau protein by improving climbing ability, evaluated by rapid iterative negative geotaxis (RING), and improving short-term memory, evaluated by a courtship conditioning assay. Cinnamaldehyde had no positive impact on the healthspan of AD flies overexpressing the Aβ42 protein.

Fluoxetine Protects against Dendritic Spine Loss in Middle-aged APPswe/PSEN1dE9 Double Transgenic Alzheimer’s Disease Mice

2020 ◽  
Vol 17 (1) ◽  
pp. 93-103 ◽  
Author(s):  
Jing Ma ◽  
Yuan Gao ◽  
Wei Tang ◽  
Wei Huang ◽  
Yong Tang
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Dendritic Spines ◽  
Dendritic Spine ◽  
Early Stage ◽  
Learning Ability ◽  
Middle Aged ◽  
Protein Levels ◽  
Spine Pathology ◽  
The Impact

Background: Studies have suggested that cognitive impairment in Alzheimer’s disease (AD) is associated with dendritic spine loss, especially in the hippocampus. Fluoxetine (FLX) has been shown to improve cognition in the early stage of AD and to be associated with diminishing synapse degeneration in the hippocampus. However, little is known about whether FLX affects the pathogenesis of AD in the middle-tolate stage and whether its effects are correlated with the amelioration of hippocampal dendritic dysfunction. Previously, it has been observed that FLX improves the spatial learning ability of middleaged APP/PS1 mice. Objective: In the present study, we further characterized the impact of FLX on dendritic spines in the hippocampus of middle-aged APP/PS1 mice. Results: It has been found that the numbers of dendritic spines in dentate gyrus (DG), CA1 and CA2/3 of hippocampus were significantly increased by FLX. Meanwhile, FLX effectively attenuated hyperphosphorylation of tau at Ser396 and elevated protein levels of postsynaptic density 95 (PSD-95) and synapsin-1 (SYN-1) in the hippocampus. Conclusion: These results indicated that the enhanced learning ability observed in FLX-treated middle-aged APP/PS1 mice might be associated with remarkable mitigation of hippocampal dendritic spine pathology by FLX and suggested that FLX might be explored as a new strategy for therapy of AD in the middle-to-late stage.

Emerging Proof of Protein Misfolding and Interactions in Multifactorial Alzheimer's Disease

2020 ◽  
Vol 20 (26) ◽  
pp. 2380-2390 ◽  
Author(s):  
Md. Sahab Uddin ◽  
Abdullah Al Mamun ◽  
Md. Ataur Rahman ◽  
Tapan Behl ◽  
Asma Perveen ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Protein Misfolding ◽  
Neurodegenerative Disorder ◽  
Senile Plaques ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Misfolded Proteins ◽  
Cell Organelles ◽  
The Impact

Objective: Alzheimer's disease (AD) is a devastating neurodegenerative disorder, characterized by the extracellular accumulations of amyloid beta (Aβ) as senile plaques and intracellular aggregations of tau in the form of neurofibrillary tangles (NFTs) in specific brain regions. In this review, we focus on the interaction of Aβ and tau with cytosolic proteins and several cell organelles as well as associated neurotoxicity in AD. Summary: Misfolded proteins present in cells accompanied by correctly folded, intermediately folded, as well as unfolded species. Misfolded proteins can be degraded or refolded properly with the aid of chaperone proteins, which are playing a pivotal role in protein folding, trafficking as well as intermediate stabilization in healthy cells. The continuous aggregation of misfolded proteins in the absence of their proper clearance could result in amyloid disease including AD. The neuropathological changes of AD brain include the atypical cellular accumulation of misfolded proteins as well as the loss of neurons and synapses in the cerebral cortex and certain subcortical regions. The mechanism of neurodegeneration in AD that leads to severe neuronal cell death and memory dysfunctions is not completely understood until now. Conclusion: Examining the impact, as well as the consequences of protein misfolding, could help to uncover the molecular etiologies behind the complicated AD pathogenesis.

scholarly journals Metabolic phenotyping reveals a reduction in the bioavailability of serotonin and kynurenine pathway metabolites in both the urine and serum of individuals living with Alzheimer’s disease

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Luke Whiley ◽  
◽  
Katie E. Chappell ◽  
Ellie D’Hondt ◽  
Matthew R. Lewis ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Systemic Inflammation ◽  
Metabolic Phenotyping ◽  
Acid Urine ◽  
Metabolite Concentrations ◽  
Ssri Medication ◽  
The Impact ◽  
Urine And Serum ◽  
Urine Serum

Abstract Background Both serotonergic signalling disruption and systemic inflammation have been associated with the pathogenesis of Alzheimer’s disease (AD). The common denominator linking the two is the catabolism of the essential amino acid, tryptophan. Metabolism via tryptophan hydroxylase results in serotonin synthesis, whilst metabolism via indoleamine 2,3-dioxygenase (IDO) results in kynurenine and its downstream derivatives. IDO is reported to be activated in times of host systemic inflammation and therefore is thought to influence both pathways. To investigate metabolic alterations in AD, a large-scale metabolic phenotyping study was conducted on both urine and serum samples collected from a multi-centre clinical cohort, consisting of individuals clinically diagnosed with AD, mild cognitive impairment (MCI) and age-matched controls. Methods Metabolic phenotyping was applied to both urine (n = 560) and serum (n = 354) from the European-wide AddNeuroMed/Dementia Case Register (DCR) biobank repositories. Metabolite data were subsequently interrogated for inter-group differences; influence of gender and age; comparisons between two subgroups of MCI - versus those who remained cognitively stable at follow-up visits (sMCI); and those who underwent further cognitive decline (cMCI); and the impact of selective serotonin reuptake inhibitor (SSRI) medication on metabolite concentrations. Results Results revealed significantly lower metabolite concentrations of tryptophan pathway metabolites in the AD group: serotonin (urine, serum), 5-hydroxyindoleacetic acid (urine), kynurenine (serum), kynurenic acid (urine), tryptophan (urine, serum), xanthurenic acid (urine, serum), and kynurenine/tryptophan ratio (urine). For each listed metabolite, a decreasing trend in concentrations was observed in-line with clinical diagnosis: control > MCI > AD. There were no significant differences in the two MCI subgroups whilst SSRI medication status influenced observations in serum, but not urine. Conclusions Urine and serum serotonin concentrations were found to be significantly lower in AD compared with controls, suggesting the bioavailability of the neurotransmitter may be altered in the disease. A significant increase in the kynurenine/tryptophan ratio suggests that this may be a result of a shift to the kynurenine metabolic route due to increased IDO activity, potentially as a result of systemic inflammation. Modulation of the pathways could help improve serotonin bioavailability and signalling in AD patients.

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