Berserker Squirrels of New York / Light Pollution Associated with Parkinson's Prevalence

This morning brought me a rather disturbing story about squirrels aggressively attacking residents of a Queens, New York neighborhood. The attacks were unprovoked. The story is reported in detail here:

 
What could cause the squirrels to behave this way? It could be due to food scarcity; there have been a lot of restaurant closures due the pandemic - so fewer scraps around and less garbage to raid.

There have been cases of people feeding meth (methamphetamine) to squirrels in order to make them more aggressive:

The other thought that comes to mind is that the behavior change could be due to SARS-CoV-2 infection. It is at least theoretically possible for squirrels to become infected and there is some preliminary evidence linking covid with onset of mental illness in humans.

The methamphetamine possibility seems more likely - but in any case, it would be prudent to trap one of the squirrels and have it examined thoroughly by a veterinarian, rather than simply assume the squirrels are just really, really hangry.

Since squirrel brains differ quite a bit from those of humans and have some fascinating features - it made me wonder if these differences, particularly in dopaminergic function, could act as a multiplier in either scenario, making for a more exaggerated response in squirrels. I tried searching on this topic and instead turned up an interesting article that explores a possible relationship between Parkinson's disease and artificial light exposure [Romeo et al. 2013]:

           https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3589725/ 

"Remarkably, in preliminary analysis that accounted for population density, the age and race adjusted Parkinson's disease prevalence significantly correlated with average satellite-observed sky light pollution. 

... lifestyle has changed in the last decades and today the majority of the general population, with the exception of some categories of workers like farmers and fishermen, spends most of the daytime indoors, at home and work, therefore it would be more appropriate to consider exposure to artificial light rather than sunlight in a correlation study with Parkinson's disease prevalence. According to this, in a correlation analysis that accounted for population density, the age- and race-adjusted Parkinson's disease prevalence significantly correlated with average satellite-observed sky light-pollution.

Together, these observations suggest that artificial light rather than sunlight could play a role in Parkinson's disease, although future spatial epidemiological analyses using an incident Parkinson's disease cohort, detailed exposure modeling, and inclusion of other potential confounders are prudent to examine this association further.

It is worth noting that the spectral characteristics of artificial light, especially fluorescent light, are completely different from sunlight, as the sunlight spectrum is continuous while fluorescent light spectrum is discontinuous and shows several peaks. Light frequencies of the sunlight spectrum could protect rather than damage the dopamine neurons, as we have mentioned above for near-infrared light. Given that, it would be worth identifying which frequency(s) of the fluorescent lamp used in our experiments is damaging the dopaminergic neurons, and to study whether other electromagnetic frequencies derived by other light sources, like computer and TV screens, are detrimental to dopamine neurons. Eventually, these findings could lead to safer light devices."
 
In addition to the epidemiological association, the paper also presents corroborating results of experiments on rats which showed an increase in neuromelanin formation in their substantia nigra after continuous light exposure. The researchers had cut the optic nerves of the rats; they hypothesized that the influence of light was through light penetrating into the rats' brains. 
 
"At the end of the light exposure period in a rat of ~400 g, the percentage of energy that crossed the scalp and the skull was about ~0.1% for the peak at 436.6 nm and ~15% for the minor peaks around 710 nm. Together, these data would suggest that external light passes through the head of the animal, reaches the substantia nigra, hits dopamine in complex with Fe3+, and triggers its auto-oxidation."
 

It seems more likely that light exposure causes the skin to release systemically circulating factors which then influence the formation of neuromelanin in the brain. Whatever the mechanism, the finding is interesting. [edit 2021-7-2: mechanism may be through the ophthalmic branch of the trigenimal nerve]

Did the method used for controlling for population density in the Romeo et al. [2013] study adequately control for factors relating to differences between urban and rural populations? If not, then there are further issues to be considered.

Regarding differences between urban and rural populations and light pollution exposure - city dwellers do not, for the most part, spend their nights roaming the streets - they go inside and turn the lights on, just as their rural counterparts do. However, rural dwellers may spend more time outdoors and so would have less artificial light exposure indoors during the day; a Canadian study found rural children and adults spent more time outdoors than urban residents, but the differences were only 0.7 and 1.2 hours more per day, respectively.

https://pubmed.ncbi.nlm.nih.gov/26566986/

Light pollution likely correlates with certain types of air pollution; results of epidemiological studies on PD and air pollution appear to be mixed.

https://www.sciencedirect.com/science/article/pii/S0160412019300984?via%3Dihub

https://pubmed.ncbi.nlm.nih.gov/30606679/

The Science of Parkinson's blog reviews recent findings regarding PM2.5, a specific type of air pollution, and PD and Alzheimer's Disease:

https://scienceofparkinsons.com/2020/10/22/pollution/

The Romeo et al. [2013] study did not account for differences in smoking rates. In the United States, smoking and tobacco use rates are higher in rural areas, rural smokers start at an earlier age and smoke more cigarettes per day than urban smokers.

https://www.cdc.gov/tobacco/disparities/geographic/index.htm

Smoking has been hypothesized to be neuroprotective of PD since epidemiological studies have found inverse associations between PD and smoking; however, Ritz et al. [2014] make the case for reverse causation:

https://pubmed.ncbi.nlm.nih.gov/25217056/

On the other hand, vegetables in the Solanaceae family (e.g., bell peppers and eggplants) contain small amounts of nicotine and their consumption is also associated with reduced PD risk.

https://pubmed.ncbi.nlm.nih.gov/23661325/

However, if causal, the effect may be due to other active constituents present in these vegetables.

"Finally, constituents of peppers other than nicotine may be neuroprotective. Given the possible interaction between PD, peppers and tobacco use, shared phytochemicals are of particular interest. Another alkyloid, anatabine, is an intriguing possibility because it has anti-inflammatory properties and might be more feasibly employed as a neuroprotective chemical than nicotine due to its longer half-life and perhaps lower toxicity and addictive potential. Alternatively, capsinoids in peppers and capsaicinoids in spicy peppers activate transient receptor potential cation channel subfamily vanilloid member 1 (TRPV1) receptors. These receptors are in the substantia nigra, and they and capsaicin may affect survival of midbrain dopaminergic neurons. Given the relatively weak results for tomatoes, it is unlikely that lycopene or vitamins A and C account for our findings."

As usual, I am left with more questions than answers.

 

 


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