The Entorhinal Cortex and Adult Neurogenesis in Major Depression

Kim, Il Bin; Park, Seon Cheol

doi:10.3390/ijms222111725

Cited by 27 publications

(21 citation statements)

References 160 publications

(186 reference statements)

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“…Li et al, 2019). Given the cellular heterogeneity of the entorhinal cortex(Kim & Park, 2021), the application of single‐cell/nucleus RNA sequencing (scRNA‐seq/snRNA‐seq) could expand our understanding of how cell types are affected during entorhinal cortex aging (J. Li et al, 2021; H. Zhang et al, 2021; W. Zhang et al, 2020).…”

Section: Introductionmentioning

confidence: 99%

Single‐cell analysis reveals transcriptomic reprogramming in aging primate entorhinal cortex and the relevance with Alzheimer's disease

Song

et al. 2022

Aging Cell

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The entorhinal cortex is of great importance in cognition and memory, its dysfunction causes a variety of neurological diseases, particularly Alzheimer's disease (AD). Yet so far, research on entorhinal cortex is still limited. Here, we provided the first single‐nucleus transcriptomic map of primate entorhinal cortex aging. Our result revealed that synapse signaling, neurogenesis, cellular homeostasis, and inflammation‐related genes and pathways changed in a cell‐type‐specific manner with age. Moreover, among the 7 identified cell types, we highlighted the neuronal lineage that was most affected by aging. By integrating multiple datasets, we found entorhinal cortex aging was closely related to multiple neurodegenerative diseases, particularly for AD. The expression levels of APP and MAPT, which generate β‐amyloid (Aβ) and neurofibrillary tangles, respectively, were increased in most aged entorhinal cortex cell types. In addition, we found that neuronal lineage in the aged entorhinal cortex is more prone to AD and identified a subpopulation of excitatory neurons that are most highly associated with AD. Altogether, this study provides a comprehensive cellular and molecular atlas of the primate entorhinal cortex at single‐cell resolution and provides new insights into potential therapeutic targets against age‐related neurodegenerative diseases.

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Section: Introductionmentioning

confidence: 99%

Single‐cell analysis reveals transcriptomic reprogramming in aging primate entorhinal cortex and the relevance with Alzheimer's disease

Song

et al. 2022

Aging Cell

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“…Traditionally, inflammation has been considered an essential response to tissue injury or microbial invasion in order to protect homeostasis. Although other pathogeneses are being actively investigated, the molecular basis of the inflammatory pathway is considered critical in the pathogenesis of psychiatric disorders, including depression [ 82 , 83 , 84 , 85 , 86 ]. Increasing evidence suggests that excessive inflammation plays a crucial role in the onset and progression of stress-related diseases.…”

Section: Stress Inflammation and Depressionmentioning

confidence: 99%

The Relationship between Stress, Inflammation, and Depression

2022

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A narrative review about the relationship between stress, inflammation, and depression is made as follows: Chronic stress leads to various stress-related diseases such as depression. Although most human diseases are related to stress exposure, the common pathways between stress and pathophysiological processes of different disorders are still debatable. Chronic inflammation is a crucial component of chronic diseases, including depression. Both experimental and clinical studies have demonstrated that an increase in the levels of pro-inflammatory cytokines and stress hormones, such as glucocorticoids, substantially contributes to the behavioral alterations associated with depression. Evidence suggests that inflammation plays a key role in the pathology of stress-related diseases; however, this link has not yet been completely explored. In this study, we aimed to determine the role of inflammation in stress-induced diseases and whether a common pathway for depression exists. Recent studies support pharmacological and non-pharmacological treatment approaches significantly associated with ameliorating depression-related inflammation. In addition, major depression can be associated with an activated immune system, whereas antidepressants can exert immunomodulatory effects. Moreover, non-pharmacological treatments for major depression (i.e., exercise) may be mediated by anti-inflammatory actions. This narrative review highlights the mechanisms underlying inflammation and provides new insights into the prevention and treatment of stress-related diseases, particularly depression.

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“…MDD was previously hypothesized to be related to monoaminergic deficiency which leads to reduced levels of monoamines at the synaptic cleft, but more recently, there has been a shift towards the "neurogenesis/neuroplasticity hypothesis of depression". Disruption of hippocampal neurogenesis in depression may be a consequence of neural circuitry impairments, in particular, the entorhinal cortex, which has a regulatory effect on the neural circuitry related to hippocampal function and adult neurogenesis (Kim and Park 2021 ; Tartt et al 2022 ). Neuromodulation and hippocampal neurogenesis that are closely related to dopamine depletion in PD, therefore, may help to elucidate the role of neurogenic-related mechanisms mediating neurotrophic processes, the role of neurogenic effects of the gene SNCA and, possibly, the molecular mechanisms underlying DPD and MDD (Flores et al 2020 ).…”

Section: Other Pathogenic Factors In Dpdmentioning

confidence: 99%

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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The Entorhinal Cortex and Adult Neurogenesis in Major Depression

Cited by 27 publications

References 160 publications

Single‐cell analysis reveals transcriptomic reprogramming in aging primate entorhinal cortex and the relevance with Alzheimer's disease

Single‐cell analysis reveals transcriptomic reprogramming in aging primate entorhinal cortex and the relevance with Alzheimer's disease

The Relationship between Stress, Inflammation, and Depression

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

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