scholarly journals Neuropsychiatric Symptoms in Patients With Alzheimer’s Disease During SARS-COV-2 Pandemic in Peru

2021 ◽  
Vol 36 ◽  
pp. 153331752110390
Author(s):  
Nilton Custodio ◽  
Sheila Castro-Suárez ◽  
Rosa Montesinos ◽  
Virgilio E. Failoc-Rojas ◽  
Rossana Cruz del Castillo ◽  
...  

To evaluate neuropsychiatric symptoms in patients with Alzheimer’s disease (AD) and their association with cognition and functionality during lockdown of the COVID-19’s first wave. We included 91 patients and caregivers of people with AD from a memory clinic. The RUDAS, M@T, and CDR were administered to patients and NPI/ADCS-ADL to caregivers. Baseline and lockdown measurements scales were analyzed to compare the frequencies at baseline versus lockdown and conditional Odds Ratio (ORc) was calculated for the neuropsychiatric symptoms. During the pandemic, significant increase in the number of cases was observed in depression (23%), agitation (36.8%), aberrant motor activity (12%), sleep disorders (26.3%), and appetite change (12.1%). In worsening of pre-existing symptoms, the most frequent were delusions (75%), followed by sleep disorders (71.7%). Lockdown induces a rapid increase of neuropsychiatric symptoms affecting cognitive symptoms and functionality of Peruvian patients with AD.

2020 ◽  
Vol 16 (S6) ◽  
Author(s):  
Willem S. Eikelboom ◽  
Michiel Coesmans ◽  
Ellen H. Singleton ◽  
Rik Ossenkoppele ◽  
John C. van Swieten ◽  
...  

2021 ◽  
Author(s):  
Willem S. Eikelboom ◽  
Esther van den Berg ◽  
Ellen Singleton ◽  
Sara J. Baart ◽  
Michiel Coesmans ◽  
...  

ABSTRACTObjectiveTo investigate the prevalence and trajectories of neuropsychiatric symptoms (NPS) in relation to cognitive functioning in a cohort of amyloid-β positive individuals across the Alzheimer’s disease (AD) clinical spectrum.MethodsWe included 1,524 amyloid-β positive individuals from the Amsterdam Dementia Cohort with subjective cognitive decline (SCD, n=113), mild cognitive impairment (MCI, n=321), or dementia (n=1,090). We measured NPS with the neuropsychiatric inventory (NPI), examining total scores and the presence of specific NPI-items. Cognition was assessed across five cognitive domains and with the MMSE. We examined trajectories including model based trends for NPS and cognitive functioning over time. We used linear mixed models to relate baseline NPI scores to cognitive functioning at baseline (whole-sample) and longitudinal time-points (subsample n=520, Mean=1.8 [SD=0.7] years follow-up).ResultsNPS were prevalent across all clinical AD stages (NPI total score ≥1 81.4% in SCD, 81.2% in MCI, 88.7% in dementia). Cognitive functioning showed an uniform gradual decline; while in contrast, large intra-individual heterogeneity of NPS was observed over time across all groups. At baseline, we found associations between NPS and cognition in dementia that were most pronounced for NPI total scores and MMSE (range β:-0.18–0.11, FDR-adjusted p<0.05), while there were no cross-sectional relationships in SCD and MCI (β:-0.32– 0.36, FDR-adjusted p>0.05). There were no associations between baseline NPS and cognitive functioning over time in any clinical stage (β:-0.13–0.44, FDR-adjusted p>0.05).ConclusionNPS and cognitive symptoms are both prevalent across the AD continuum, but show a different evolution during the course of the disease.


2019 ◽  
Vol 3 (Supplement_1) ◽  
pp. S857-S857
Author(s):  
Weizhou Tang

Abstract Behavioral and psychological symptoms (BPS) represent a heterogeneous group of non-cognitive symptoms occurring in persons with Alzheimer’s disease (PwAD), and they are often associated with negative outcomes for AD caregivers. Evidence indicates differences in caregivers’ mental health across race/ethnic groups. However, there is a lack of research that compares racial differences in BPS in PwAD. This study aims to compare racial differences in BPS in PwAD and caregiver depression. The study analyzed data collected from the South Carolina AD Registry in 2010. The survey used in the interview included measures of caregiver depression, caregiver burden, PwAD’s non-cognitive symptoms, caregiving competence, caregiver distress, and demographics. The final analysis focused on 635 African-American (n=313) and white (n=322) caregivers. Mann-Whitney U-tests, Chi-square tests, and multiple linear regression were conducted. Among all PwAD, higher percentage of whites than African Americans exhibited apathy/indifference (67.52% vs 52.44%, p=.0001), depression/dysphoria (61.54% vs 44.59%, p&lt;.0001), and anxiety (45.08% vs 29.64%, p&lt;.0001). In terms of both frequency and severity of BPS, whites had significantly higher BPS score (Mean=35.49, SD=24.75) than African Americans (Mean=28.13, SD=23.97; p&lt;.0001). Mean comparisons indicated significant group differences in caregiver depressive symptoms between white caregivers (mean=11.89, SD=6.90) and African-American caregivers (mean=9.41, SD=5.77). However, there were no racial differences in the relationship between BPS in PwAD and caregiver depression. The findings of this study highlight the importance of developing more effective and targeted treatment options and therapies for neuropsychiatric symptoms and delivering cultural relevant education programs/interventions to ethnic groups.


2019 ◽  
Vol 216 (1) ◽  
pp. 1-3 ◽  
Author(s):  
George Savulich ◽  
John T. O'Brien ◽  
Barbara J. Sahakian

SummaryAlzheimer's disease and vascular dementia are associated with overlapping symptoms of anxiety and depression. More accurate discrimination between emerging neuropsychiatric and cognitive symptoms would better assist illness detection. The potential for protection against cognitive decline and dementia following early identification and intervention of neuropsychiatric symptoms warrants investigation.


2016 ◽  
Vol 12 ◽  
pp. P688-P690
Author(s):  
Paulina Lebrija ◽  
Maria Fernanda Alarcon ◽  
Ana Luisa Sosa-Ortiz ◽  
Gilberto Isaac Acosta-Castillo ◽  
Rocio Ramirez-Santos

Author(s):  
Zeba Mueed ◽  
Pankaj Kumar Rai ◽  
Mohammad A. Kamal ◽  
Nitesh Kumar Poddar

Alzheimer’s disease (AD), characterized by abnormally phosphorylated tau, paired helical filaments (PHFs), neurofibrillary tangles (NFTs), deregulated mammalian target of rapamycin (mTOR), Aβ deposits, is a multifactorial disease with sleep disorders being one of the causative agents. Therefore, we have reviewed the literature and have tried to decode the existence of positive feedback, reciprocal and a bidirectional relationship allying between sleep disturbances and AD. Much light has been thrown on the role of tau pathology and amyloid pathology in sleep pathology and its association with AD pathology. We have also discussed the role of melatonin in regulating sleep disorders and AD. The neuroprotective action of melatonin via inhibiting tau hyperphosphorylation and Aβ deposition has also been pondered upon. Moreover, astrocytes involvement in aggravating AD has also been highlighted in this review. Several therapeutic approaches aimed at improving both sleep disorders and AD have been duly discussed such as administration of antidepressants and antihistamines, immunotherapy, metal chelators, melatonin supplementation, light therapy and physical activity. Despite consistent efforts, the complete etiology concerning sleep disorder and AD is still unclear. Therefore, further research is needed to unravel the mechanism involved and also to develop strategies that may help in obstructing AD in its preclinical stage.


2021 ◽  
Vol 14 (5) ◽  
pp. 458
Author(s):  
Barbara Miziak ◽  
Barbara Błaszczyk ◽  
Stanisław J. Czuczwar

Alzheimer’s disease (AD; progressive neurodegenerative disorder) is associated with cognitive and functional impairment with accompanying neuropsychiatric symptoms. The available pharmacological treatment is of a symptomatic nature and, as such, it does not modify the cause of AD. The currently used drugs to enhance cognition include an N-methyl-d-aspartate receptor antagonist (memantine) and cholinesterase inhibitors. The PUBMED, Medical Subject Heading and Clinical Trials databases were used for searching relevant data. Novel treatments are focused on already approved drugs for other conditions and also searching for innovative drugs encompassing investigational compounds. Among the approved drugs, we investigated, are intranasal insulin (and other antidiabetic drugs: liraglitude, pioglitazone and metformin), bexarotene (an anti-cancer drug and a retinoid X receptor agonist) or antidepressant drugs (citalopram, escitalopram, sertraline, mirtazapine). The latter, especially when combined with antipsychotics (for instance quetiapine or risperidone), were shown to reduce neuropsychiatric symptoms in AD patients. The former enhanced cognition. Procognitive effects may be also expected with dietary antioxidative and anti-inflammatory supplements—curcumin, myricetin, and resveratrol. Considering a close relationship between brain ischemia and AD, they may also reduce post-brain ischemia neurodegeneration. An investigational compound, CN-105 (a lipoprotein E agonist), has a very good profile in AD preclinical studies, and its clinical trial for postoperative dementia is starting soon.


2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Adeline Su Lyn Ng ◽  
Juan Wang ◽  
Kwun Kei Ng ◽  
Joanna Su Xian Chong ◽  
Xing Qian ◽  
...  

Abstract Background Alzheimer’s disease (AD) and behavioral variant frontotemporal dementia (bvFTD) cause distinct atrophy and functional disruptions within two major intrinsic brain networks, namely the default network and the salience network, respectively. It remains unclear if inter-network relationships and whole-brain network topology are also altered and underpin cognitive and social–emotional functional deficits. Methods In total, 111 participants (50 AD, 14 bvFTD, and 47 age- and gender-matched healthy controls) underwent resting-state functional magnetic resonance imaging (fMRI) and neuropsychological assessments. Functional connectivity was derived among 144 brain regions of interest. Graph theoretical analysis was applied to characterize network integration, segregation, and module distinctiveness (degree centrality, nodal efficiency, within-module degree, and participation coefficient) in AD, bvFTD, and healthy participants. Group differences in graph theoretical measures and empirically derived network community structures, as well as the associations between these indices and cognitive performance and neuropsychiatric symptoms, were subject to general linear models, with age, gender, education, motion, and scanner type controlled. Results Our results suggested that AD had lower integration in the default and control networks, while bvFTD exhibited disrupted integration in the salience network. Interestingly, AD and bvFTD had the highest and lowest degree of integration in the thalamus, respectively. Such divergence in topological aberration was recapitulated in network segregation and module distinctiveness loss, with AD showing poorer modular structure between the default and control networks, and bvFTD having more fragmented modules in the salience network and subcortical regions. Importantly, aberrations in network topology were related to worse attention deficits and greater severity in neuropsychiatric symptoms across syndromes. Conclusions Our findings underscore the reciprocal relationships between the default, control, and salience networks that may account for the cognitive decline and neuropsychiatric symptoms in dementia.


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