Covid-19 might be escalating the onset of Parkinson’s disease, say researchers

Researchers have suggested a that there may be a causal relationship between Parkinson’s disease and Covid-19.

Already established long-term hangovers of the Covid-19 are starting to become well documented, and are mainly focused on the potentially separate series of complications known colloquially and collectively as long Covid. But additional conditions have also been attributed to acute-virial infection in older patients – namely chronic pain, sarcopenia, malnutrition, depression, and delirium.

Academics have argued that treatment for these long-term conditions could possibly have consequential future ramifications – especially if the virus is not adequately suppressed, or if we merely “take it on the chin” as the Prime Minister said in March – and herd immunity becomes rediscussed as the political goal.

Is Covid-19 creating “a perfect storm” for the development of Parkinson’s Disease?

New research, although limited in its scope, has suggested that another health complication to add to the list attributed to Covid-19 could be the development of, or the rapid escalation of symptoms related to, Parkinson’s disease.

Parkinson’s disease currently is one of the fastest growing neurological conditions in the world, and in the UK, around 145,000 people are living with the condition and a further 18,000 are diagnosed every year, according to Parkinson’s UK.

Intriguingly researcher referenced three published single-case reports that have documented the development of clinical parkinsonism in three patients aged 35, 45, and 58.

Notably the researchers said that these three cases studies of parkinsonism do not prove a causal relationship between Covid-19 and the development of symptoms, as potentially those three patients were already destined to develop parkinsonism.

Although they also said that the rapid manifestation of symptoms post exposure to the virus is worth consideration – especially as a Covid-19 post-mortem study discovered immune response cytotoxic T cells in the brainstem – which is a neuropathological sign associated with Parkinson disease.

Researches suggested three scenarios, that could work independently of each other or in conjunction, for the rapid development of parkinsonism:

1. Vascular damage in combination with thick, blood clot prone sticky blood – both of which has been a feature of this virus – resulting in brain damage which is seen in vascular parkinsonism.
2. Due to the association of inflammatory disorders and Parkinson disease, researchers said that it is possible that inflammation caused by acute-Covid-19 could trigger neuroinflammation.
3. Covid-19 might be a neurotropic virus, as viral RNA has been detected post-mortem. And as hyposmia (partial or complete loss of smell) is a common feature of Parkinson’s and Covid-19 – that suggests similar affected brain regions. Additionally, research suggests that viral infections can increase the production of the alpha-synuclein protein which possibly can lead to neuronal death. The report emphases that if this is correct long-term systemic and/or neuro-inflammation due to Covid-19, might be “a perfect storm” for the development of PD’.

While this research could be accused of unscientific conjecture – as the individual case studies are so far limited – it does however point to future research, and developments.