Is depression a neurological disorder?

Depression is not solely a neurological disorder, but it has strong neurological components.

While I believe that neurological aspects play a critical role, I first became depressed due to social and psychological difficulties escalating my genetic vulnerabilities. I needed to get my anxiety and insecurities under control while learning some essential skills to allow me to feel better again and to do well in life once more.

It’s more accurate to describe it as a multifactorial mental health disorder that involves a combination of biological, psychological, and social factors (often called the biopsychosocial model).

Neurological aspects of depression

From a neurological perspective, depression involves:

1. Brain structure and function

• • Studies using fMRI and PET scans depict changes in brain regions like the prefrontal cortex, amygdala, hippocampus, and anterior cingulate cortex.

• • For example, hippocampal shrinkage is often seen in people with recurrent or chronic depression.

2. Neurotransmitter dysregulation

• • Imbalances in serotonin, dopamine, norepinephrine, and GABA have been associated with depressive symptoms.

• • However, the “chemical imbalance” theory is oversimplified. It’s more about how these systems interact and regulate mood over time.

3. Neuroplasticity and BDNF

• • Depression is linked to reduced levels of brain-derived neurotrophic factor (BDNF), which supports neuron growth and connectivity.

• • Antidepressants may help by boosting BDNF levels and promoting neuroplasticity.

4. Neuroinflammation

• • Increased levels of pro-inflammatory cytokines like IL-6 and TNF-alpha have been discovered in some people with depression.

• • Chronic inflammation may affect neurotransmission and add to depressive symptoms.

5. Cognitive impairment and executive dysfunction

• • People with depression often experience difficulties with attention, working memory, decision-making, and cognitive flexibility.

• • These deficits are linked to dysfunction in the prefrontal cortex and frontostriatal circuits, which are critical for executive function.

• • Many still show residual cognitive impairment even in remission, suggesting persistent neurological effects.

I had a lot of trouble concentrating and remembering information at my worst, and it took a long time to subside, even though I was feeling and doing better.

6. Default mode network (DMN) dysregulation

• • The default mode network is a brain network active during rest and self-referential thinking (like daydreaming or rumination).

• • The DMN becomes overactive and poorly regulated, especially during tasks that should deactivate it.

• • This contributes to excessive rumination.

7. Altered brain connectivity

• • Depression is increasingly seen as a network-level disorder instead of just an imbalance in a single region.

• • Studies using fMRI and DTI (diffusion tensor imaging) illustrate disrupted functional and structural connectivity between major brain regions.

• • The connections between the prefrontal cortex, limbic system (like the amygdala), and reward pathways are most affected.

8. Reward system hypofunction (anhedonia)

• • Depression is often marked by anhedonia, or reduced ability to experience pleasure.

• • This links closely to dysfunction in the brain’s reward system.

• • Neuroimaging shows blunted activity in response to rewarding stimuli, even in people who are not currently feeling “sad.”

9. Epigenetic changes in the brain

• • Chronic stress and depression can trigger changes in gene expression without altering the DNA sequence itself (epigenetic modifications).

• • For example, changes in histone acetylation or DNA methylation affect how genes involved in neuroplasticity and mood regulation are expressed.

• • This may partly explain why early life trauma can have long-lasting effects on brain function and depression risk.

10. Sleep architecture disruption

• • People with depression often have altered REM sleep patterns, including:

• • • Decreased REM latency (faster onset of REM).

• • • Increased REM density.

• • • Broken sleep cycles.

• • These patterns hint at dysfunction in brainstem structures and circadian regulation, which are neurologically mediated.

I was regularly unable to fall asleep and would frequently wake up during the night when I managed to.

11. Response to neuromodulation therapies

• • Treatments like transcranial magnetic stimulation (TMS) and electroconvulsive therapy (ECT) work by directly modifying brain activity in areas like the dorsolateral prefrontal cortex.

• • Their effectiveness in treatment-resistant depression is strong evidence that brain circuits play a causal role, not just a correlation.

Beyond the brain: Why it’s not just neurological

1. Genetics

There’s a heritable component, but no single “depression gene.”

It’s inheritable and interacts with life experiences.

2. Stress and trauma

Chronic stress alters the HPA axis (hypothalamic-pituitary-adrenal) and contributes to mood dysregulation.

3. Psychosocial factors

Loss, isolation, unemployment, or childhood adversity play a major role in triggering or sustaining depression.

I started withdrawing from friends and family because of my problems, which aggravated my mood issues even more.

Conclusion

While depression has a clear neurological basis, calling it purely a neurological disorder would miss the full picture.

It’s a complex disorder where the brain, body, and environment interact with each other.

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