The effects of cognitive reserve and depressive symptoms on cognitive performance in major depression and bipolar disorder

Ponsoni, André; Branco, Laura Damiani; Cotrena, Charles; Shansis, Flávio; Fonseca, Róchele Paz

doi:10.1016/j.jad.2020.05.143

Cited by 16 publications

(5 citation statements)

References 48 publications

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“…Cognitive disorders mediated couple depression in the largest proportion among significant mediating variables. Recently, the Rotterdam study reported that higher cognitive reserve, defined as the common variance across cognitive tests, may be a protective factor for late-life depression, which is in line with several previous studies that suggested that low cognitive reserve may increase the risk of late-life depression. Cognitive and brain reserve coping mechanisms are particularly important in regions that are related to neuromodulation of the serotonin system .…”

Section: Discussionsupporting

confidence: 83%

Shared Risk Factors for Depressive Disorder Among Older Adult Couples in Korea

et al. 2023

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ImportanceAlthough couples may share many risk factors for depressive disorders in their lifetime, whether these factors mediate the shared risk of depressive disorders has rarely been investigated.ObjectivesTo identify the shared risk factors for depressive disorder in couples and investigate their mediating roles in the shared risk of depressive disorders among older adult couples.Design, Setting, and ParticipantsThis nationwide, multicenter, community-based cohort study assessed 956 older adults from the Korean Longitudinal Study on Cognitive Aging and Dementia (KLOSCAD) and a cohort of their spouses (KLOSCAD-S) between January 1, 2019, to February 28, 2021.ExposuresDepressive disorders of the KLOSCAD participants.Main Outcomes and MeasuresThe mediating roles of shared factors in couples on the association between one spouse’s depressive disorder and the other’s risk of depressive disorders was examined using structural equation modeling.ResultsA total of 956 KLOSCAD participants (385 women [40.3%] and 571 men [59.7%]; mean [SD] age, 75.1 [5.0] years) and their spouses (571 women [59.7%] and 385 men [40.3%]; mean [SD] age, 73.9 [6.1] years) were included. The depressive disorders of the KLOSCAD participants were associated with an almost 4-fold higher risk of depressive disorders in their spouses in the KLOSCAD-S cohort (odds ratio, 3.89; 95% CI, 2.06-7.19; P &lt; .001). Social-emotional support mediated the association between depressive disorders in the KLOSCAD participants and their spouses’ risk of depressive disorders by itself (β = 0.012; 95% CI, 0.001-0.024; P = .04; mediation proportion [MP] = 6.1%) and through chronic illness burden (β = 0.003; 95% CI, 0.000-0.006; P = .04; MP = 1.5%). Chronic medical illness burden (β = 0.025; 95% CI, 0.001-0.050; P = .04; MP = 12.6%) and presence of a cognitive disorder (β = 0.027; 95% CI, 0.003-0.051; P = .03; MP = 13.6%) mediated the association.Conclusions and RelevanceThe risk factors shared by older adult couples may mediate approximately one-third of the spousal risk of depressive disorders. Identification of and intervention in the shared risk factors of depression among older adult couples may reduce the risk of depressive disorders in the spouses of older adults with depression.

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Section: Discussionsupporting

confidence: 83%

Shared Risk Factors for Depressive Disorder Among Older Adult Couples in Korea

et al. 2023

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“…Non-amnestic MCI, likely caused by vascular pathology, is a protective factor for the reversal of MCI to normal cognitive functioning, suggesting a potential reversibility of the unfavorable synergistic effect of depression and vascular risk factors. Reducing depression reduces white matter hyperintensity pathology in the brain and the adverse effect on cognitive reserve, reducing the likelihood of MCI (68)(69)(70). The potential effect of psychotherapy and cognitive stimulating activities on the prevention and treatment of MCI (126)(127)(128) has so far been insufficiently studied.…”

Section: Discussionmentioning

confidence: 99%

Uloga depresije u razvoju blagog kognitivnog poremećaja

Perhoč Mrla,

Jurin

2024

SOC PSIH

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Blagi kognitivni poremećaj (BKP) smatra se stanjem između zdravog starenja i demencije, različitih etioloških čimbenika, kliničkih prezentacija i progresivnosti profila. Cilj rada je dati cjelovit pregled spoznaja o ulozi depresije u razvoju BKP-a. Značajna povezanost depresije s incidencijom BKP-a potvrđena je u većini istraživanja. Depresija može biti rizični čimbenik za razvoj BKP-a. Povezanost depresije i BKP-a ostvaruje se i zajedničkim čimbenicima -vaskularnim lezijama, patologijom Alzheimerove demencije (AD), genetskom vezom. Depresivni simptomi i promjene bijele tvari mogu imati aditivni ili sinergistički učinak za razvoj BKP-a. Rizični čimbenici za incidenciju BKP-a u depresivnih osoba su starija životna dob, kumulativni depresivni simptomi, dulje trajanje depresije, veći intenzitet depresivnih simptoma, niska, ali i visoka zastupljenost patologije AD-a, sinergistička aditivna interakcija nedostatka tjelesne aktivnosti i poteškoća spavanja, depresije i anksioznosti, muški rod, niži stupanj formalnog obrazovanja, aktualno posjedovanje recepta za korištenje antidepresiva. Zaštitni čimbenici koji pospješuju reverziju u uredno kognitivno funkcioniranje u depresivnih osoba su mlađa dob, neamnestički BKP, manji intenzitet depresivnih simptoma ili pak smanjenje depresivnih simptoma. / Mild cognitive impairment (MCI) is understood as a condition between normal aging and dementia, with different etiological factors, clinical presentations and progression profiles. The aim of this paper was to provide a comprehensive overview of the role of depression in the development of MCI. Most studies have confirmed that there is a significant connection between depression and the incidence of MCI. Depression can be a risk factor for the development of MCI. The connection between depression and MCI is achieved through common factors such as vascular lesions, Alzheimer's diseasepathology and genetic links. Depressive symptoms and changes in white matter may have an additive or synergistic effect on the development of MCI. Risk factors for the incidence of MCI in individuals with depression include older age, cumulative depressive symptoms, longer duration of depression, higher severity of depressive symptoms, low, but also high burden of Alzheimer's pathology, synergistic additive interaction of lack of physical activity and sleep difficulties, depression and anxiety, male gender, lower level of formal education and current prescription of antidepressants. Protective factors that promote the reversion to normal cognitive functioning in depressed individuals include younger age, non-amnestic MCI, lower severity of depressive symptoms or a reduction in depressive symptoms.

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“…First, the pathogenetic causes of both memory deficits and depression were different, i.e., depression was not necessarily sufficient to impair the memory function of the brain [49]. Second, the brain damage caused by sE2 was not sufficient to affect the neuronal circuits responsible for memory [50,51].…”

Section: Discussionmentioning

confidence: 99%

Supraphysiologic doses of 17β-estradiol aggravate depression-like behaviors in ovariectomized mice possibly via regulating microglial responses and brain glycerophospholipid metabolism

Li,

Zhang,

Chen

et al. 2023

J Neuroinflammation

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Background 17β-Estradiol (E2) is generally considered neuroprotective in humans. However, the current clinical use of estrogen replacement therapy (ERT) is based on the physiological dose of E2 to treat menopausal syndrome and has limited therapeutic efficacy. The efficacy and potential toxicity of superphysiological doses of ERT for menopausal neurodegeneration are unknown. Methods In this study, we investigated the effect of E2 with a supraphysiologic dose (0.5 mg/kg, sE2) on the treatment of menopausal mouse models established by ovariectomy. We performed the open field, Y-maze spontaneous alternation, forced swim tests, and sucrose preference test to investigate behavioral alterations. Subsequently, the status of microglia and neurons was detected by immunohistochemistry, HE staining, and Nissl staining, respectively. Real-time PCR was used to detect neuroinflammatory cytokines in the hippocampus and cerebral cortex. Using mass spectrometry proteomics platform and LC–MS/ MS-based metabolomics platform, proteins and metabolites in brain tissues were extracted and analyzed. BV2 and HT22 cell lines and primary neurons and microglia were used to explore the underlying molecular mechanisms in vitro. Results sE2 aggravated depression-like behavior in ovariectomized mice, caused microglia response, and increased proinflammatory cytokines in the cerebral cortex and hippocampus, as well as neuronal damage and glycerophospholipid metabolism imbalance. Subsequently, we demonstrated that sE2 induced the pro-inflammatory phenotype of microglia through ERα/NF-κB signaling pathway and downregulated the expression of cannabinoid receptor 1 in neuronal cells, which were important in the pathogenesis of depression. Conclusion These data suggest that sE2 may be nonhelpful or even detrimental to menopause-related depression, at least partly, by regulating microglial responses and glycerophospholipid metabolism.

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The effects of cognitive reserve and depressive symptoms on cognitive performance in major depression and bipolar disorder

Cited by 16 publications

References 48 publications

Shared Risk Factors for Depressive Disorder Among Older Adult Couples in Korea

Shared Risk Factors for Depressive Disorder Among Older Adult Couples in Korea

Uloga depresije u razvoju blagog kognitivnog poremećaja

Supraphysiologic doses of 17β-estradiol aggravate depression-like behaviors in ovariectomized mice possibly via regulating microglial responses and brain glycerophospholipid metabolism

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