Does Prozac damage brain cells? (+3 evidences)

In this article, we will discuss whether the use of Prozac can cause brain cell damage. Prozac is a selective serotonin reuptake inhibitor (SSRI). In addition to its effect on serotonin levels, Prozac can promote neurogenesis and alter pathways involved in neural plasticity and neuronal survival.

Does Prozac damage brain cells?

Yes, Prozac is known to cause damage to brain cells. The long-term use of Prozac can lead to brain damage and neurological agitations. However, no sign of brain injury or loss of intellectual capacity is observed in patients taking Prozac for a shorter time. 

Chronic Prozac exposure alters the expression of genes involved in myelination, a process that regulates brain connectivity. The long-term use of Prozac can also cause a shift in fatty acid metabolism. Lipids help in the formation of cell membranes and are required for normal brain function. Deficiencies and abnormalities in fatty acid metabolism can lead to brain damage.

On the flip side, an International joint study revealed that persistent depression causes brain damage rather than Prozac being a risk factor for it. Some clinical and animal studies have suggested that Prozac can protect against cerebral ischaemia. 

What is the potential effect of Prozac on the brain cells?

Several gene expression experiments in rodents have revealed that, in addition to the serotogenic systems, SSRIs like Prozac can alter a wide range of pathways. Adult SSRI drugs can change gene expression levels of hypothalamic hormones, neurotrophic factors, components of non-serotogenic neurotransmitters, and inflammatory factors.

Downregulation of proinflammatory cytokines can limit HPA axis function (facilitating stress reduction), enhance serotonin (5-HT) and dopamine production, and inhibit 5-HT and dopamine absorption (1, 2). 

Critically, 5-HT functions as a neurotransmitter throughout development. In particular, 5-HT regulates neurodevelopmental processes such as neuron migration and brain formation during the early stages of development (2).

What does the animal experimental data suggest?

Exposure to SSRIs during brain development has been shown to disrupt the formation of the myelin sheath in rats. Additionally, there is evidence that Prozac can alter the microstructure of white matter during adulthood, which is primarily made up of myelinated axons (3).

In one of the studies, when Prozac was administered in adult and neonatal rats, the regulation of Cntf, a neurotrophic factor involved in myelination, revealed an opposing pattern in the adults. There was a negative correlation between the expression of genes related to myelination and anxiety-like behaviour. The authors concluded that long-term exposure to Prozac results in alterations in the expression of genes related to myelination, a process that modifies brain connectivity (4).

In another study, 10mg/kg of Prozac provided after global cerebral ischemia reduced neuronal damage. Although long-term neuroprotection requires more research, the authors’ findings imply that Prozac may have therapeutic potential and neuroprotective effects when given after cerebral ischaemia, cardiac arrest, and cardiopulmonary resuscitation (5). 

In a study conducted on mice, Prozac inhibited apoptotic cell death in hippocampus neurons as well as vascular endothelial cell death while improving learning and memory. The author’s finding suggested that Prozac’s neuroprotective effect is likely mediated by blocking matrix metalloproteases (MMP) activation following blood-brain barrier (BBB) disruption after transient global ischemia. Thus, Prozac may be a potential therapeutic agent for preserving BBB integrity following ischemic brain injury (6).

How does Prozac alter the brain structure in humans?

In a case report, a patient with OCD was treated with Prozac after a brain injury. The investigators observed a reduced quantity of serotonin neurons emerging from the raphe nuclei and lesions in the orbital-frontal circuits, which are implicated in OCD following traumatic brain injury (7).

In a preliminary pilot study, patients who were administered 40 mg/day of Prozac showed a decrease in choline was assessed in grey matter tissue after the first and second weeks of administration. The apparent diffusion coefficient was raised in white matter lesions at week one and N-acetyl aspartate was increased in the second week.

The observed partial normalization of the structure-related Magnetic Resonance Spectroscopy (MRS) parameter in white matter lesions provided evidence of Prozac’s neuroprotective effect in multiple sclerosis (8).  

What are the long-term effects of Prozac on the brain?

Prozac is generally administered for months or years at a time. It has an energizing effect that usually becomes apparent during the first few weeks. These new effects can be felt almost immediately. Long-term use of Prozac can cause brain damage and the patient might experience symptoms like neurological agitation, suicidal thoughts, panic attacks, anxiety, and mood changes. 

Prozac’s long-term effects last much beyond the initial few days or weeks of medication. In one of the case reports, prolonged use of Prozac led to tic (tongue darting in and out of the mouth) in a female patient. The condition persisted even when the drug was discontinued. The involuntary and disfiguring symptoms included: 

  • Lip puckering,
  • lip-smacking,
  • fish-like kissing motions, and
  • pelvic thrusting.

What are the mitigation plans for Prozac-induced brain damage?

Caring for a person who has suffered brain damage due to Prozac can impose greater difficulties on the patient and their family members. It will be beneficial if family members:

  • Have enough knowledge of the impacts of acquired brain damage,
  • recognise the obstacles that may arise in the life of the patient,
  • accept that rehabilitation is a slow process.

Depending upon the severity of brain damage, the patient might be referred to a neurologist or a physiotherapist.

Considering the benefits vs. risks of Prozac

Despite the black box warning for increased suicidal thoughts, Prozac is the only SSRI that is not prohibited for children. This signifies that the advantages of using Prozac exceed its risks and side effects. 

Long-term Prozac use can cause damage to brain cells or decrease memory and psychomotor function. However, short-term use reduces the occurrence of such changes. Therefore, it is important to comply with the dosage regimen and slowly taper off the medication when needed.


It is important to consult your healthcare provider if you are on long-term treatment of Prozac and happen to experience any abnormal behaviour. Never take any side effects casually and always comply with the follow-up plan with your healthcare provider.

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Alme MN, Wibrand K, Dagestad G, Bramham CR. Chronic fluoxetine treatment induces brain region-specific upregulation of genes associated with BDNF-induced long-term potentiation. Neural plasticity. 2007 Oct;2007.


Fan Q, Yan X, Wang J, Chen Y, Wang X, Li C, Tan L, You C, Zhang T, Zuo S, Xu D. Abnormalities of white matter microstructure in unmedicated obsessive-compulsive disorder and changes after medication. PloS one. 2012 Apr 27;7(4):e35889.


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