Are there Sex Differences in Emotional and Biological Responses in Spousal Caregivers of Patients with Alzheimer’s Disease?

2004 ◽  
Vol 5 (4) ◽  
pp. 319-330 ◽  
Author(s):  
Russel (Trey) L. Thompson ◽  
Sharon L. Lewis ◽  
Margaret R. Murphy ◽  
Jennifer M. Hale ◽  
Paula H. Blackwell ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Nk Cell ◽  
Physiological Stress ◽  
Muscle Tension ◽  
Cell Number ◽  
Coping Resources ◽  
Spousal Caregivers ◽  
Activated T Cells ◽  
Biological Responses

The purpose of this study was to compare emotional and biological responses of men and women who are spousal caregivers of patients with Alzheimer’s disease (AD). Quality-of-life measurements, bioinstrumentation data, and immunophenotype assessments were obtained from female and male spousal caregivers of patients with AD. Spousal caregivers (women, n = 45 with average age 69.7; men, n = 16 with average age 71.4 years) completed questionnaires that assessed psychosocial variables. Blood was drawn and lymphocyte subsets (including natural killer [NK] cell number) were determined using flow cytometry. The degree of relaxation was determined measuring muscle tension (EMG) in the frontalis and trapezius muscles, skin conductance, skin temperature, and heart rate. Male spousal caregivers, as compared to female spousal caregivers, had significantly lower levels of stress, depression, caregiver burden (subjective), anxiety, anger-hostility, and somatic symptoms and higher levels of mental health, sense of coherence, NK cell number, and social and physical functioning. There were no statistically significant differences between the 2 groups in social support, coping resources, or T, T suppressor, or activated T cells. Women had more T helper cells and fewer NK cells than men. Men had fewer manifestations of a physiological stress response, as indicated by bioinstrumentation parameters. Unique sex-specific issues need to be considered when strategies are implemented to assist the increasing number of caregivers as our society ages.

scholarly journals Immunosenescence of Natural Killer Cells, Inflammation, and Alzheimer’s Disease

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Corona Solana ◽  
Raquel Tarazona ◽  
Rafael Solana
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Nk Cells ◽  
Natural Killer ◽  
Nk Cell ◽  
Neurodegenerative Disorder ◽  
The Elderly ◽  
Lymphoid Cells ◽  
Target Cells ◽  
The Brain

Alzheimer’s disease (AD) represents the most common cause of dementia in the elderly. AD is a neurodegenerative disorder characterized by progressive memory loss and cognitive decline. Although the aetiology of AD is not clear, both environmental factors and heritable predisposition may contribute to disease occurrence. In addition, inflammation and immune system alterations have been linked to AD. The prevailing hypothesis as cause of AD is the deposition in the brain of amyloid beta peptides (Aβ). Although Aβ have a role in defending the brain against infections, their accumulation promotes an inflammatory response mediated by microglia and astrocytes. The production of proinflammatory cytokines and other inflammatory mediators such as prostaglandins and complement factors favours the recruitment of peripheral immune cells further promoting neuroinflammation. Age-related inflammation and chronic infection with herpes virus such as cytomegalovirus may also contribute to inflammation in AD patients. Natural killer (NK) cells are innate lymphoid cells involved in host defence against viral infections and tumours. Once activated NK cells secrete cytokines such as IFN-γ and TNF-α and chemokines and exert cytotoxic activity against target cells. In the elderly, changes in NK cell compartment have been described which may contribute to the lower capacity of elderly individuals to respond to pathogens and tumours. Recently, the role of NK cells in the immunopathogenesis of AD is discussed. Although in AD patients the frequency of NK cells is not affected, a high NK cell response to cytokines has been described together with NK cell dysregulation of signalling pathways which is in part involved in this altered behaviour.

scholarly journals Cell number changes in Alzheimer's disease relate to dementia, not to plaques and tangles

Brain ◽  
2013 ◽  
Vol 136 (12) ◽  
pp. 3738-3752 ◽  
Author(s):  
C. H. Andrade-Moraes ◽  
A. V. Oliveira-Pinto ◽  
E. Castro-Fonseca ◽  
C. G. da Silva ◽  
D. M. Guimaraes ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cell Number

scholarly journals Fingolimod Rescues Memory and Improves Pathological Hallmarks in the 3xTg-AD Model of Alzheimer’s Disease

2022 ◽  
Author(s):  
Steven G. Fagan ◽  
Sibylle Bechet ◽  
Kumlesh K. Dev
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Biochemical Analysis ◽  
Spatial Working Memory ◽  
Cell Number ◽  
Model Of Alzheimer’S Disease ◽  
Candidate Drug ◽  
Inflammatory Processes ◽  
The Brain ◽  
Ad Mouse Model

AbstractTherapeutic strategies for Alzheimer’s disease (AD) have largely focused on the regulation of amyloid pathology while those targeting tau pathology, and inflammatory mechanisms are less explored. In this regard, drugs with multimodal and concurrent targeting of Aβ, tau, and inflammatory processes may offer advantages. Here, we investigate one such candidate drug in the triple transgenic 3xTg-AD mouse model of AD, namely the disease-modifying oral neuroimmunomodulatory therapeutic used in patients with multiple sclerosis, called fingolimod. In this study, administration of fingolimod was initiated after behavioral symptoms are known to emerge, at 6 months of age. Treatment continued to 12 months when behavioral tests were performed and thereafter histological and biochemical analysis was conducted on postmortem tissue. The results demonstrate that fingolimod reverses deficits in spatial working memory at 8 and 12 months of age as measured by novel object location and Morris water maze tests. Inflammation in the brain is alleviated as demonstrated by reduced Iba1-positive and CD3-positive cell number, less ramified microglial morphology, and improved cytokine profile. Finally, treatment with fingolimod was shown to reduce phosphorylated tau and APP levels in the hippocampus and cortex. These results highlight the potential of fingolimod as a multimodal therapeutic for the treatment of AD.

Visual Communication to Improve Relationship Quality in Spousal Caregivers of Individuals With Alzheimer's Disease

2019 ◽  
pp. 59-76
Author(s):  
Nola Freeman
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Relationship Quality ◽  
Case Studies ◽  
Art Therapy ◽  
Visual Communication ◽  
Spousal Caregivers ◽  
Positive Interactions ◽  
Couple Dynamics ◽  
Therapy Interventions

The study investigated the effectiveness of an art therapy intervention in improving relationship quality of spousal caregivers and their spouses with Alzheimer's Disease (AD). Two single case studies were conducted, each composed of a caregiver and spouse with AD. Intervention consisted of three art therapy sessions based on visual communication, or the mutual creation of artwork. Relationship quality was measured throughout the study using clinical notes, pretest and posttest, and caregiver daily reports of positive interactions with their spouse. Couple dynamics were found to influence how positively each art therapy directive was viewed; however, both caregivers noted valuing art therapy interventions for providing recreation and socialization. The intervention resulted in increased positive interactions in both case studies.

scholarly journals The Pathological Roles of Ganglioside Metabolism in Alzheimer's Disease: Effects of Gangliosides on Neurogenesis

2011 ◽  
Vol 2011 ◽  
pp. 1-14 ◽  
Author(s):  
Toshio Ariga ◽  
Chandramohan Wakade ◽  
Robert K. Yu
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Β ◽  
Cholinergic Neurons ◽  
Cell Number ◽  
Neuronal Membrane ◽  
Amyloid Β Protein ◽  
Neuroepithelial Cells ◽  
Ganglioside Metabolism ◽  
Membrane Components

Conversion of the soluble, nontoxic amyloid β-protein (Aβ) into an aggregated, toxic form rich in β-sheets is a key step in the onset of Alzheimer's disease (AD). It has been suggested that Aβ induces changes in neuronal membrane fluidity as a result of its interactions with membrane components such as cholesterol, phospholipids, and gangliosides. Gangliosides are known to bind Aβ. A complex of GM1 and Aβ, termed “GAβ”, has been identified in AD brains. Abnormal ganglioside metabolism also may occur in AD brains. We have reported an increase of Chol-1α antigens, GQ1bα and GT1aα, in the brain of transgenic mouse AD model. GQ1bα and GT1aα exhibit high affinities to Aβs. The presence of Chol-1α gangliosides represents evidence for genesis of cholinergic neurons in AD brains. We evaluated the effects of GM1 and Aβ1–40 on mouse neuroepithelial cells. Treatment of these cells simultaneously with GM1 and Aβ1–40 caused a significant reduction of cell number, suggesting that Aβ1–40 and GM1 cooperatively exert a cytotoxic effect on neuroepithelial cells. An understanding of the mechanism on the interaction of GM1 and Aβs in AD may contribute to the development of new neuroregenerative therapies for this disorder.

scholarly journals Arginase Inhibition Supports Survival and Differentiation of Neuronal Precursors in Adult Alzheimer’s Disease Mice

2020 ◽  
Vol 21 (3) ◽  
pp. 1133 ◽  
Author(s):  
Baruh Polis ◽  
Kolluru D. Srikanth ◽  
Vyacheslav Gurevich ◽  
Naamah Bloch ◽  
Hava Gil-Henn ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transgenic Mice ◽  
Adult Neurogenesis ◽  
Progenitor Cell ◽  
Molecular Mechanisms ◽  
Neuronal Cell ◽  
Cell Number ◽  
Wild Type ◽  
Newborn Neuron

Adult neurogenesis is a complex physiological process, which plays a central role in maintaining cognitive functions, and consists of progenitor cell proliferation, newborn cell migration, and cell maturation. Adult neurogenesis is susceptible to alterations under various physiological and pathological conditions. A substantial decay of neurogenesis has been documented in Alzheimer’s disease (AD) patients and animal AD models; however, several treatment strategies can halt any further decline and even induce neurogenesis. Our previous results indicated a potential effect of arginase inhibition, with norvaline, on various aspects of neurogenesis in triple-transgenic mice. To better evaluate this effect, we chronically administered an arginase inhibitor, norvaline, to triple-transgenic and wild-type mice, and applied an advanced immunohistochemistry approach with several biomarkers and bright-field microscopy. Remarkably, we evidenced a significant reduction in the density of neuronal progenitors, which demonstrate a different phenotype in the hippocampi of triple-transgenic mice as compared to wild-type animals. However, norvaline showed no significant effect upon the progenitor cell number and constitution. We demonstrated that norvaline treatment leads to an escalation of the polysialylated neuronal cell adhesion molecule immunopositivity, which suggests an improvement in the newborn neuron survival rate. Additionally, we identified a significant increase in the hippocampal microtubule-associated protein 2 stain intensity. We also explore the molecular mechanisms underlying the effects of norvaline on adult mice neurogenesis and provide insights into their machinery.

scholarly journals Oxytocin cell number in the human paraventricular nucleus remains constant with aging and in Alzheimer's disease

1991 ◽  
Vol 12 (5) ◽  
pp. 511-516 ◽  
Author(s):  
M. Wierda ◽  
E. Goudsmit ◽  
P.F. Van Der Woude ◽  
J.S. Purba ◽  
M.A. Hofman ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Paraventricular Nucleus ◽  
Cell Number

Impact of Behavioural Problems on Spousal Caregivers: A Comparison between Alzheimer’s Disease and Frontotemporal Dementia

2006 ◽  
Vol 22 (1) ◽  
pp. 35-41 ◽  
Author(s):  
Marjolein E. de Vugt ◽  
Samantha R. Riedijk ◽  
Pauline Aalten ◽  
Aad Tibben ◽  
John C. van Swieten ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Frontotemporal Dementia ◽  
Spousal Caregivers ◽  
Behavioural Problems

Decreasing sense of coherence and its determinants in spousal caregivers of persons with mild Alzheimer's disease in three year follow-up: ALSOVA study

2014 ◽  
Vol 26 (7) ◽  
pp. 1211-1220 ◽  
Author(s):  
Tarja Välimäki ◽  
Janne Martikainen ◽  
Kristiina Hongisto ◽  
Mikael Fraunberg ◽  
Ilona Hallikainen ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Sense Of Coherence ◽  
Female Gender ◽  
Drop Out ◽  
Spousal Caregivers ◽  
Efficacy Parameters ◽  
Support Programmes ◽  
Relationship Of

ABSTRACTBackground:Sense of coherence (SOC) is associated with the capability to cope with caregiving. Our aims were (1) to describe the trajectory of SOC in aged spousal caregivers of persons with mild Alzheimer's disease (AD) in 3-year follow-up and (2) to identify baseline determinants influencing SOC change.Methods:Both AD (n = 170) (CDR-SOB, MMSE, NPI, ADCS-ADL) and caregiver- (n = 170) (BDI, SOC) related efficacy parameters were evaluated annually. Follow-up time was 3 years. The relationship of potential baseline factors with longitudinal SOC was analyzed using linear mixed models.Results:The mean drop-out-adjusted SOC score (148.5 at baseline) was decreased by 4.56 points (p = 0.002) during the follow-up. Caregivers’ depression at baseline predicted the significant decrease of SOC (every + 1 BDI point decreases 2.181 points in SOC, p = 0.0001). When caregiver's depression was not taken into account in the analysis, female gender, and higher age and AD patient's lower baseline MMSE were associated significantly (p < 0.05) with decreasing SOC score in the follow-up. Other studied covariates were not associated with SOC change.Conclusions:SOC is not as stable as expected, but decreases during long-lasting caregiving. Caregiver's depression at baseline predicts SOC decrease over time. In the future, caregiver dependent factors should be evaluated at the beginning of caregiving to target individualized support programmes to the vulnerable caregivers.

Sign in / Sign up

Export Citation Format

Share Document