The enigma of vascular depression in old age: a critical update

Ka, Jellinger

doi:10.1007/s00702-022-02521-5

Cited by 12 publications

(10 citation statements)

References 190 publications

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“…Studies had shown that paroxetine and citalopram remain the safest drugs because of their minimal bleeding risk and inhibition of metabolic enzymes (CYP450)( Electroconvulsive therapy (ECT) can induce seizures through the scalp to pray for a certain therapeutic effect on PSD. Transcranial direct current stimulation (tDCS) involved the use of shallow electrical currents to stimulate speci c brain regions that had been found to be very helpful in depression (Jellinger, 2022). Neuromodulation via repetitive transcranial magnetic stimulation (rTMS) involved the non-invasive repetitive generation of magnetic pulses followed by electric elds that induce speci c brain regions.When low-frequency rTMS (1HZ) was applied to the left anterolateral prefrontal cortex, the study found improvements in patients' mood and cognitive function, and the observed side effects were smaller than those observed with ECT (Valiengo et al, 2022).…”

Section: Group 4: Treatment Research For Post-stroke Depressionmentioning

confidence: 99%

Bibliometric analysis of global research trends in post-stroke depression: hotspots and frontiers

Yang

et al. 2023

Preprint

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Background Post-stroke depression(PSD) is one of the most common complications of stroke which affects recovery and quality of patients’ life adversely. PSD also is a significant source of burden for caregivers. Recently, the number of publications on PSD has been an increasing worldwide that means PSD has attracted more and more attention. Therefore, a more comprehensive understanding of the publications on PSD is now required. The purpose of this paper is to analyze the research status, discover the hotspots and frontiers about PSD. Methods The publications’ raw data was retrieved from the Web of Science Core Collection on September 19, 2022. Impact Factor (IF) and Journal Citation Reports (JCR) segments of the publications were obtained from the Web of Science website. Visualization analysis was performed on CiteSpace and VOSviewer. Results From 2012 to 2022, the number of citations and publications about PSD increased exponentially year by year. Finally, a total of 3268 publications related to PSD were identified. China (867) and the US (738) had the most publications; Capital Med Univ and Univ Melbourne were the most prolific institutions. Ungvari GS and Hackett ML were the most active authors and the most prolific and co-cited, respectively. Journal of stroke cerebrovascular diseases (131 articles) was the highest output. Among the 3268 publications, International journal of stroke had the most citations (43.9 times), Stroke has the most citations (2,990) and the highest H-index value. The citation burst for 8 co-cited references lasts until 2022. Finally, this paper divided the hot spots into four categories: cluster 1 (study on risk factors of PSD), cluster 2 (clinically relevant research on PSD), cluster 3 (mechanisms of PSD), and cluster 4 (the Treatment Study for PSD). Conclusion PSD research is one research main area worldwide. This work demonstrated the knowledge structure and the evolution of the PSD research field and predictdresearches trends through visual analysis. The study of clinical treatment and prevention of PSD will instead of the study of the mechanism in the future. This study provides reference for future research of PSD.

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Section: Group 4: Treatment Research For Post-stroke Depressionmentioning

confidence: 99%

Bibliometric analysis of global research trends in post-stroke depression: hotspots and frontiers

Yang

et al. 2023

Preprint

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“…Neuroimaging and neuropathological studies have provided insight into important pathobiological mechanisms of DPD, suggesting that it is associated with a more widespread neurodegenerative process, involving subcortical dopaminergic, serotonergic and noradrenergic nuclei and pathways (Maillet et al 2021 ; Remy et al 2005 ). However, as the loss of neural populations also underlies cognitive impairment, it may be difficult to differentiate the clinical effects of such neurodegeneration in early phases of depression in PD from those of early dementias, although both may occur together (Di Giuda et al 2012 ; Jellinger 2022b ). Although the diagnosis of PD relies on the effects of dopamine deficiency, it is associated with other neurotransmitter deficits that are causing various motor and non-motor signs and symptoms, e.g., depression (Jones et al 2019 ; Schapira et al 2017 ).…”

Section: Dysfunction Of Neurotransmitter Systemsmentioning

confidence: 99%

“…Since PD causes depletion of dopaminergic neurons in the SN, depression may be part of the pathophysiological process that leads to PD. Widespread degeneration of dopaminergic terminals in the striatum, particularly in dorsal caudate, is seen in PD patients with both depression and mild cognitive impairment, with relative preservation of the other dopaminergic systems in the brain (Jellinger 2022b ).…”

Section: Dopaminergic Systemmentioning

confidence: 99%

“…Whereas vascular risk factors failed to verify the vascular depression hypothesis in PD (Ou et al 2018 ), others suggested that co-morbid cerebral small-vessel disease (CSVD), marked by WM hypointensity, number of lacunes and microbleeds, may affect multiple functional domains in PD, including motor, cognitive and emotional impairments (Chen et al 2021 ). Many studies have provided evidence that large WM hypointensity volumes, subcortical lacunes and other markers for CSVD are associated with increased risk for depressive symptoms (Geraets et al 2021 ; Jellinger 2021 , 2022b ; Nunes et al 2022 ; Wang et al 2020 ), since they are disturbing cortico-subcortical neuronal circuits causing microstructural dysfunctions of major brain connections involved in emotion and other important behaviors, thus suggesting an association between CSVD and depression (Empana et al 2021 ; Kim and Han 2021 ; Nunes et al 2022 ).…”

Section: Other Pathogenic Factors In Dpdmentioning

confidence: 99%

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The pathobiological basis of depression in Parkinson disease: challenges and outlooks

Ka¹

2022

J Neural Transm

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Depression, with an estimated prevalence of about 40% is a most common neuropsychiatric disorder in Parkinson disease (PD), with a negative impact on quality of life, cognitive impairment and functional disability, yet the underlying neurobiology is poorly understood. Depression in PD (DPD), one of its most common non-motor symptoms, can precede the onset of motor symptoms but can occur at any stage of the disease. Although its diagnosis is based on standard criteria, due to overlap with other symptoms related to PD or to side effects of treatment, depression is frequently underdiagnosed and undertreated. DPD has been related to a variety of pathogenic mechanisms associated with the underlying neurodegenerative process, in particular dysfunction of neurotransmitter systems (dopaminergic, serotonergic and noradrenergic), as well as to disturbances of cortico-limbic, striato-thalamic-prefrontal, mediotemporal-limbic networks, with disruption in the topological organization of functional mood-related, motor and other essential brain network connections due to alterations in the blood–oxygen-level-dependent (BOLD) fluctuations in multiple brain areas. Other hypothetic mechanisms involve neuroinflammation, neuroimmune dysregulation, stress hormones, neurotrophic, toxic or metabolic factors. The pathophysiology and pathogenesis of DPD are multifactorial and complex, and its interactions with genetic factors, age-related changes, cognitive disposition and other co-morbidities awaits further elucidation.

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“…Several, partially overlapping etiological factors for these disruptions have been discussed, including vascular mechanisms, inflammation, neuroimmune regulatory dysfunction, neurodegenerative changes, and amyloid accumulation (for recent reviews, see Alexopoulos, 2019 ; Jellinger, 2022 ). Another highly consistent finding in LLD is the observation of white matter lesions (WMLs), which are recognizable as hyperintense on T2-weighted images and which are predominantly caused by ischemic changes in small vessels ( van Agtmaal et al, 2017 ).…”

Section: Introductionmentioning

confidence: 99%

The need to change: Is there a critical role of midlife adaptation in mental health later in life?

Thams

Brassen

2023

eLife

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Although late-life depression (LLD) is a serious health problem and more common than dementia in people over 60, it is underdiagnosed and undertreated. The cognitive-emotional etiology of LLD is particularly poorly understood. This is in contrast to the now extensive literature from psychology and cognitive neuroscience on the characteristics of emotionally healthy aging. This research consistently shows a change in emotional processing in older adults that is modulated by prefrontal regulation. Lifespan theories explain this change in terms of neurocognitive adaptation to limited opportunities and resources that typically occur in the second half of life. Epidemiological data on an increase in well-being after a low point around age 50 suggest that the majority of people seem quite capable of making this adaptation, even though empirical evidence for a causal modulation of this so called ‘paradox of aging’ and for the role of the midlife dip is still lacking. Intriguingly, LLD is associated with deficits in emotional, cognitive, and prefrontal functions similar to those shown to be crucial for healthy adaptation. Suspected causes of these deficits, such as white matter lesions or affective instability, become apparent as early as midlife when internal and external changes as well as daily challenges set in. Based on these findings, we propose that some individuals who develop depression at older ages may not have been able to successfully implement self-regulatory adaptation at midlife. Here, we review the current evidence and theories on successful aging, the neurobiology of LLD, and well-being across the lifespan. Drawing on recent advances in lifespan theories, emotion regulation research, and cognitive neuroscience, we propose a model of successful versus unsuccessful adaptation that emphasizes the increasing need for implicit habitual control and resource-based regulatory choice during midlife.

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The enigma of vascular depression in old age: a critical update

Cited by 12 publications

References 190 publications

Bibliometric analysis of global research trends in post-stroke depression: hotspots and frontiers

Bibliometric analysis of global research trends in post-stroke depression: hotspots and frontiers

The pathobiological basis of depression in Parkinson disease: challenges and outlooks

The need to change: Is there a critical role of midlife adaptation in mental health later in life?

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