Long Covid May Involve Injury to Dopamine-producing Neurons in Brain: Study
The finding, published in the journal eBioMedicine, may explain symptoms such as lack of motivation due to fatigue, slowed movement, and memory difficulties, and could open the door to new treatment strategies
By : PTI
Update: 2026-07-13 12:01 GMT
New Delhi: A new study has put forth the strongest evidence to date that long COVID, in which neurological symptoms of COVID-19 such as brain fog and fatigue persist beyond the acute infection period, could be associated with an injury to dopamine-releasing neurons in the brain.
The finding, published in the journal eBioMedicine, may explain symptoms such as lack of motivation due to fatigue, slowed movement, and memory difficulties, and could open the door to new treatment strategies, researchers said.
Researchers, led by those at the Centre for Addiction and Mental Health in Canada, used positron emission tomography (PET) brain imaging to measure a well-established marker of dopamine neuron integrity in 24 people with long COVID and 43 healthy individuals.
Compared to healthy individuals, people with long COVID showed significantly lower levels of the imaging marker, indicating a reduced dopamine nerve endings density, across all major regions of the striatum -- the brain structure that plays a central role in motivation, movement and thinking.
Lower levels of the markers in the ventral striatum were specifically associated with a greater loss of motivation, while marker reductions in the dorsal putamen were associated with a slowed movement speed, and a marker loss in the caudate putamen was linked to memory difficulties.
The study represents a notable shift in how long COVID may be understood and treated, the researchers said.
Previous studies predominantly focused on brain inflammation and immune changes that occur during long COVID, with almost no clinical trials targeting the dopamine-releasing neurons, they added.
"These results indicate that long COVID is, at least in part, a disorder of the brain's dopamine system," senior author Dr Jeffrey Meyer, senior scientist at the Brain Health Imaging Centre, Centre for Addiction and Mental Health, said.
"This suggests that repurposing medications that augment the function of dopamine-releasing neurons, including dopamine precursors and inhibitors of dopamine metabolism, could be a promising approach," Dr Meyer said.
The authors wrote: "Loss of dopamine nerve terminals may be contributing to symptom correlates of apathy, motor slowing and memory decline suggesting improved function of dopaminergic synapses as a new therapeutic direction to treat long COVID."
The findings build on the team's earlier work showing that people with long COVID have elevated levels of inflammation in the brain, especially in regions that are rich in dopamine-releasing neurons.
"Our findings provide compelling evidence that long COVID involves the loss of dopamine-releasing neurons," Dr. Meyer said.
"This kind of injury is well known to produce symptoms like lack of motivation and motor slowing, and may contribute to memory difficulties in other neurological conditions. Our results suggest a similar process is occurring in long COVID," the senior author said.