Changes in Principal Caregiver Mood Affects the Mood of the Parkinson's Disease Patient: The Vicious Cycle of Illness.
Ontology highlight
ABSTRACT:
SUBMITTER: Santos-Garcia D
PROVIDER: S-EPMC10041425 | biostudies-literature | 2023
REPOSITORIES: biostudies-literature
Publications
Changes in Principal Caregiver Mood Affects the Mood of the Parkinson's Disease Patient: The Vicious Cycle of Illness.
Santos-García Diego D de Deus Fonticoba Teresa T Cores Bartolomé Carlos C Feal Painceiras Maria J MJ Íñiguez-Alvarado Maria Cristina MC García Díaz Iago I Jesús Silvia S Buongiorno Maria Teresa MT Planellas Lluís L Cosgaya Marina M García Caldentey Juan J Caballol Nuria N Legarda Ines I Hernández Vara Jorge J Cabo Iria I López Manzanares Lydia L González Aramburu Isabel I Ávila Rivera Maria A MA Gómez Mayordomo Víctor V Nogueira Víctor V Puente Víctor V Dotor García-Soto Julio J Borrué Carmen C Solano Vila Berta B Álvarez Sauco María M Vela Lydia L Escalante Sonia S Cubo Esther E Carrillo Padilla Francisco F Martínez Castrillo Juan C JC Sánchez Alonso Pilar P Alonso Losada Maria G MG López Ariztegui Nuria N Gastón Itziar I Kulisevsky Jaime J Menéndez González Manuel M Seijo Manuel M Rúiz Martínez Javier J Valero Caridad C Kurtis Mónica M González Ardura Jessica J Alonso Redondo Ruben R Ordás Carlos C López Díaz Luis M LM McAfee Darrian D Martinez-Martin Pablo P Mir Pablo P
Journal of Parkinson's disease 20230101 2
Similar Datasets
Project description:The human genetic code encrypted in thousands of genes holds the secret for synthesis of proteins that drive all biological processes necessary for normal life and death. Though the genetic ciphering remains unchanged through generations, some genes get disrupted, deleted and or mutated, manifesting diseases, and or disorders. Current treatment options-chemotherapy, protein therapy, radiotherapy, and surgery available for no more than 500 diseases-neither cure nor prevent genetic errors but often cause many side effects. However, gene therapy, colloquially called "living drug," provides a one-time treatment option by rewriting or fixing errors in the natural genetic ciphering. Since gene therapy is predominantly a viral vector-based medicine, it has met with a fair bit of skepticism from both the science fraternity and patients. Now, thanks to advancements in gene editing and recombinant viral vector development, the interest of clinicians and pharmaceutical industries has been rekindled. With the advent of more than 12 different gene therapy drugs for curing cancer, blindness, immune, and neuronal disorders, this emerging experimental medicine has yet again come in the limelight. The present review article delves into the popular viral vectors used in gene therapy, advances, challenges, and perspectives.
| S-EPMC6491712 | biostudies-literature
Project description:Epigenetic alterations, including DNA methylation and post translational modifications to histones, drive tumorigenesis and metastatic progression. In the context of bone metastasis, epigenetic modifications in tumor cells can modulate dissemination of cancer cells to the bone, tumor progression in the bone marrow, and may be associated with patient survival rates. Bone disseminated tumor cells may enter a dormant state or stimulate osteolysis through the "vicious cycle" of bone metastasis where bone disseminated tumor cells disrupt the bone microenvironment, which fuels tumor progression. Epigenetic alterations may either exacerbate or abrogate the vicious cycle by regulating tumor suppressors and oncogenes, which alter proliferation of bone-metastatic cancer cells. This review focuses on the specific epigenetic alterations that regulate bone metastasis, including DNA methylation, histone methylation, and histone acetylation. Here, we summarize key findings from researchers identifying epigenetic changes that drive tumor progression in the bone, along with pre-clinical and clinical studies investigating the utility of targeting aberrant epigenetic alterations to treat bone metastatic cancer.
| S-EPMC10830514 | biostudies-literature
Project description:BackgroundThe ambiguity of defining hope impacts the level of readiness faced by health care professionals treating patients with glioma, a disease with unpredictable outcomes. This study describes the report of hope and the relationship between hope and mood in adult brain tumor patients at various points in the illness trajectory.MethodsThis was a cross-sectional study with data collection including use of the Herth Hope Index (HHI), the Profile of Mood States-Short Form (POMS-SF), and clinical information. Descriptive statistics were used to report sample characteristics. Spearman's rho and Mann-Whitney tests were used to compare and differentiate scores.ResultsEighty-two patients ranging in age from 22 to 78 years (median, 44.5 y) participated in the study. Patients were primarily male (57.3%), married (76.8%), and had a high-grade glioma (35.4%). Nearly half had recurrence, and more than 20% were on active treatment. The overall HHI total score for the sample was 41.32 (range: 13-48). Patients with recurrence had a lower HHI interconnectedness (median = 14.00) score and higher total mood disturbance (median = 14.00) compared with patients without recurrence (median = 15.00 and median = 0.00, respectively; P < .05). All negative mood states on the POMS-SF were negatively correlated with HHI subscales.ConclusionsOverall, patients reporting more hope also reported less overall mood disturbance As expected, patients with tumor recurrence reported lower hope and higher mood disturbance than those who were newly diagnosed or without recurrence. Targeting interventions specifically tailored to an individual's needs for improvement in quality of life throughout the disease course may include measures to address hope in order to facilitate positive coping strategies.
| S-EPMC4677410 | biostudies-literature
Project description:Parkinson's disease (PD) is the second most common neurodegenerative disorder, affecting millions each year. Most PD cases (∼90%) are sporadic, resulting from the age-dependent accumulation of pathogenic effects. One key pathological hallmark of PD progression is the accumulation of alpha-synuclein (α-syn), which has been shown to negatively affect neuronal function and viability. Here, using 3- and 6-month-old Nrf2+/+ and Nrf2-/- mice overexpressing human α-syn (PD model), we show that loss of NRF2 increases markers of ferroptosis across PD-relevant brain regions. Increased ferroptosis was associated with an age- and genotype-dependent increase in α-syn pathology and behavioral deficits. Finally, we demonstrate that α-syn overexpression sensitizes neuronal cells and ex vivo brain slices to ferroptosis induction, which may be due to α-syn decreasing NRF2 protein levels. Altogether, these results indicate that NRF2 is a critical anti-ferroptotic mediator of neuronal survival, and that the vicious cycle of α-syn overexpression and NRF2 suppression, leading to enhanced neuronal ferroptotic cell death, could represent a targetable and currently untapped means of preventing PD onset and progression.
| S-EPMC9841923 | biostudies-literature
Project description:β-amyloid (Aβ)-dependent neuronal hyperactivity is believed to contribute to the circuit dysfunction that characterizes the early stages of Alzheimer's disease (AD). Although experimental evidence in support of this hypothesis continues to accrue, the underlying pathological mechanisms are not well understood. In this experiment, we used mouse models of Aβ-amyloidosis to show that hyperactivation is initiated by the suppression of glutamate reuptake. Hyperactivity occurred in neurons with preexisting baseline activity, whereas inactive neurons were generally resistant to Aβ-mediated hyperactivation. Aβ-containing AD brain extracts and purified Aβ dimers were able to sustain this vicious cycle. Our findings suggest a cellular mechanism of Aβ-dependent neuronal dysfunction that can be active before plaque formation.
| S-EPMC6690382 | biostudies-literature
Project description:Levodopa-carbidopa intestinal gel (LCIG) has shown to be efficacious in motor and non-motor symptoms (NMS). Nevertheless, studies with patient Quality of Life (QoL) as a primary endpoint are scarce. To assess the effect of LCIG on Advanced Parkinson's Disease (APD) patients QoL. Secondarily, the impact on motor symptoms and NMS, emotional well-being, treatment satisfaction, and caregiver QoL, stress, disease burden, anxiety, depression, and work impairment were also investigated. In this prospective, 6-month multicenter postmarketing observational study, LCIG was administered to 59 patients with APD. Endpoints were assessed using validated scales and questionnaires. LCIG significantly improved patient QoL (PDQ-39 mean change ± standard deviation from baseline, -12.8 ± 14.6; P < 0.0001), motor symptoms (UPDRS-III in "On," -6.5 ± 11.8; P = 0.0002), NMS (NMSS, -35.7 ± 31.1; P < 0.0001), mood (Norris/Bond-Lader VAS, -6.6 ± 21.1; P = 0.0297), fatigue (PFS-16, -0.6 ± 1.0; P = 0.0003), depression (BDI-II, -5.1 ± 9.4; P = 0.0002), anxiety (BAI, -6.2 ± 9.6; P < 0.0001), and patient treatment satisfaction (SATMED-Q, 16.1 ± 16.8; P < 0.0001). There were significant correlations between the change from baseline to 6 months between PDQ-39 and UPDRS-IV, NMSS, BAI, BDI-II, AS, and PFS-16 scores, and Norris/Bond-Lader alertness/sedation factor. Caregiver anxiety also improved (Goldberg anxiety scale, -1.1 ± 1.0; P = 0.0234), but the clinical relevance of this finding is questionable. The serious adverse events reported were similar to those previously described for LCIG. In patients with APD, LCIG improves QoL, motor symptoms and NMS, emotional well-being, and satisfaction with the treatment. Improvement in patient QoL is associated with improvements in motor complications, NMS, anxiety, depression, apathy and fatigue. Improvements in patients' QoL does not correspond with improvements in caregivers' QoL or burden.
| S-EPMC8633325 | biostudies-literature
Project description:Family caregivers play an integral role in supporting patient self-management, yet how they perform this role is unclear. We conducted a qualitative metasynthesis of family caregivers' processes to support patient self-management of chronic, life-limiting illness and factors affecting their support. Methods included a systematic literature search, quality appraisal of articles, data abstraction, and data synthesis to produce novel themes. Thirty articles met inclusion criteria, representing 935 international family caregivers aged 18 to 89 years caring for patients with various health conditions. Three themes characterized family caregivers' processes to support patient self-management: "Focusing on the Patient's Illness Needs," "Activating Resources to Support Oneself as the Family Caregiver," and "Supporting a Patient Living with a Chronic, Life-Limiting Illness." Factors affecting family caregivers' support included Personal Characteristics, Health Status, Resources, Environmental Characteristics, and the Health Care System. The family caregiver role in supporting patient self-management is multidimensional, encompassing three processes of care and influenced by multiple factors.
| S-EPMC8114560 | biostudies-literature
Project description:Fuchs endothelial corneal dystrophy (FECD) is the most common primary corneal endothelial dystrophy and the leading indication for corneal transplantation worldwide. FECD is characterized by the progressive decline of corneal endothelial cells (CECs) and the formation of extracellular matrix (ECM) excrescences in Descemet's membrane (DM), called guttae, that lead to corneal edema and loss of vision. FECD typically manifests in the fifth decades of life and has a greater incidence in women. FECD is a complex and heterogeneous genetic disease where interaction between genetic and environmental factors results in cellular apoptosis and aberrant ECM deposition. In this review, we will discuss a complex interplay of genetic, epigenetic, and exogenous factors in inciting oxidative stress, auto(mito)phagy, unfolded protein response, and mitochondrial dysfunction during CEC degeneration. Specifically, we explore the factors that influence cellular fate to undergo apoptosis, senescence, and endothelial-to-mesenchymal transition. These findings will highlight the importance of abnormal CEC-DM interactions in triggering the vicious cycle of FECD pathogenesis. We will also review clinical characteristics, diagnostic tools, and current medical and surgical management options for FECD patients. These new paradigms in FECD pathogenesis present an opportunity to develop novel therapeutics for the treatment of FECD.
| S-EPMC7648733 | biostudies-literature
Project description:Recently, we face a surge in the fast-forward Coronavirus Disease 2019 (COVID-19) pandemic with nearly 170 million confirmed cases and almost 3.5 million confirmed deaths at the end of May 2021. Obesity, also known as the pandemic of the 21st century, has been evolving as an adverse prognostic marker. Obesity is associated with a higher risk of being SARS-CoV-2-positive (46%), as well as hospitalization (113%) and death (48%) due to COVID-19. It is especially true for subjects with morbid obesity. Also, observational studies suggest that in the case of COVID-19, no favorable "obesity paradox" is observed. Therefore, it is postulated to introduce a new entity, i.e., coronavirus disease-related cardiometabolic syndrome (CIRCS). In theory, it applies to all stages of COVID-19, i.e., prevention, acute proceedings (from COVID-19 diagnosis to resolution or three months), and long-term outcomes. Consequently, lifestyle changes, glycemic control, and regulation of the renin-angiotensin-aldosterone pathway have crucial implications for preventing and managing subjects with COVID-19. Finally, it is crucial to use cardioprotective drugs such as angiotensin-converting enzyme inhibitors/angiotensin II receptor blockers and statins. Nevertheless, there is the need to conduct prospective studies and registries better to evaluate the issue of obesity in COVID-19 patients.
| S-EPMC8258476 | biostudies-literature
Project description:Bone is one of the preferential target organs of cancer metastasis. Bone metastasis is associated with various complications, of which bone pain is most common and debilitating. The cancer-associated bone pain (CABP) is induced as a consequence of increased neurogenesis, reprogramming and axonogenesis of sensory nerves (SNs) in harmony with sensitization and excitation of SNs in response to the tumor microenvironment created in bone. Importantly, CABP is associated with increased mortality, of which precise cellular and molecular mechanism remains poorly understood. Bone is densely innervated by autonomic nerves (ANs) (sympathetic and parasympathetic nerves) and SNs. Recent studies have shown that the nerves innervating the tumor microenvironment establish intimate communications with tumors, producing various stimuli for tumors to progress and disseminate. In this review, our current understanding of the role of SNs innervating bone in the pathophysiology of CABP will be overviewed. Then the hypothesis that SNs facilitate cancer progression in bone will be discussed in conjunction with our recent findings that SNs play an important role not only in the induction of CABP but also the progression of bone metastasis using a preclinical model of CABP. It is suggested that SNs are a critical component of the bone microenvironment that drives the vicious cycle between bone and cancer to progress bone metastasis. Suppression of the activity of bone-innervating SNs may have potential therapeutic effects on the progression of bone metastasis and induction of CABP.
| S-EPMC8411232 | biostudies-literature