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Explore the heterogeneity of major depressive disorder and find the best tools to study this complex disorder.
Major depressive disorder (MDD) is a clinically and biologically heterogeneous disorder, which is thought to originate from the interaction of susceptibility genes and noxious environmental events such as chronic stress. Although MDD is one of the most common debilitating mental disorders, its etiology and pathophysiology remain unclear.
The clinical heterogeneity in MDD together with a lack of knowledge on the pathophysiology hinder the diagnosis and the effective treatment of this disorder. Currently, MDD is diagnosed using a symptom-based approach; there is no non-invasive and quantitative test available1.
The investigation of mechanisms underlying MDD has been complicated by the following obstacles:
Several possible pathophysiological mechanisms of depression have been suggested, including altered neurotransmission, hypothalamus-pituitary-adrenal (HPA) axis abnormalities involved in chronic stress, inflammation, reduced neuroplasticity, and network dysfunction2.
Both glutamatergic and GABAergic neurotransmissions seem to play an important role in the pathogenesis of MDD. Accumulating evidence has demonstrated that the dysfunction of glutamatergic neurotransmission, particularly via N-methyl-d-aspartate (NMDA) receptors, contributes to the neurobiology of MDD. Several studies have revealed an altered expression of NMDA receptor subtypes and impaired NMDA receptor-mediated intracellular signaling pathways in brain circuits of patients with MDD. Furthermore, NMDA receptor antagonists, particularly ketamine, have been shown to exhibit rapid antidepressant effects in treatment-resistant depression in clinical studies3.
Inhibitory neurotransmitter γ-aminobutyric acid (GABA) has also been implicated in the pathophysiology of MDD. Studies have demonstrated a reduction in GABA levels in the brain, decreased expression of GABAergic interneuron markers, and alterations in GABAA and GABAB receptor levels in patients with MDD and chronically stressed animals4,5.
Study the involvement of NMDA receptors, GABA, and other key players in MDD with our interactive poster.
To support your research in MDD, we’ve compiled a list of our best-selling antibodies against key targets in MDD.
Gene name | Target name | Recommended abID | Publications | Applications | Suitable for |
CLDN5 | Claudin 5 | Li C 2019 | WB, IHC-P | Mouse, Human | |
GRIN2A | NMDAR2A | Lin L 2019, | WB | Mouse, Rat, Human | |
TNFAIP3 | A2 / TNFAIP3 | Liu K 2018 | ICC/IF, WB, IHC-P, Flow Cyt | Mouse, Human | |
NR3C1 | Glucocorticoid receptor | WB, IHC-P, ICC/IF, Flow Cyt | Mouse, Rat, Human | ||
HTR1A | 5HT1A receptor | Cui WQ 2019, (15 in total) | WB, IHC-P, ICC/IF | Mouse, Rat, Human | |
RELN | Reelin | NA | IHC-P | Mouse, Rat, Human |
The diagnosis of MDD currently relies on clinical examination and subjective evaluation of depressive symptoms. No approved biomarker is available as part of the diagnostic criteria despite multiple studies that have been carried out to assess various biomarkers for MDD. Identification of biomarkers in MDD could help facilitate the diagnosis of the disorder, choose the optimal treatment, and predict the treatment response as well as the course of the disorder6.
Suggested biomarkers for MDD include growth factors, cytokines and other inflammatory markers, oxidative stress markers, endocrine markers, energy balance hormones, genetic and epigenetic features, and neuroimaging6.
The most investigated growth factor in MDD is BDNF, which regulates neural plasticity, migration, and survival in the central and peripheral nervous systems. Multiple studies and meta-analyses have consistently reported that plasma and serum BDNF levels are reduced in patients with depression but can be normalized by antidepressant drugs or electroconvulsive therapy6.
In the table below, we summarize potential biomarkers for MDD.
Biomarker candidate | Source | Biomarker levels compared to healthy individuals | Product recommendations |
BDNF | Serum and plasma | Decreased | |
IL-1 | Serum and peripheral mRNA expressions | Increased | |
IL-6 | Serum and peripheral mRNA expressions | Increased | |
TNF | Serum and peripheral mRNA expressions | Increased | |
MDA | - | Increased | |
HPA activity | - | Increased | NA |
Cortisol response to DEX/CRH | - | Increased | NA |
Hippocampus volume | - | Decreased | NA |
BDNF: brain-derived neurotrophic factor, IL: interleukin, TNF: Tumor necrosis factor, MDA: malondialdehyde, HPA: hypothalamus-pituitary-adrenal, DEX/CRH: dexamethasone/corticotropin-releasing hormone.