Could zombies actually exist? What would it take for human corpses to rise up and hunt the living? We often think zombies are scientifically impossible — but actually, they’re just very implausible. Here’s one wayThe Walking Dead could happen in real life.

To start our zombie thought experiment, we need to make some basic assumptions. First, we’re ignoring all supernatural zombie origins. We’re also going to set aside space radiation, mysterious comets, or Russian satellites. Our focus will be narrowed to biological origins –- a zombie contagion. Of course, there are many different zombie scenarios in books and film, and no one theory is going to cover all of them perfectly.

The first aspect of human zombification we need to tackle is basic zombie physiology. In virtually every zombie scenario, zombies are able to function despite increasing levels of physical deterioration due to injury or decomposition. There has to be some mechanism for transmitting neural impulses from the brain to various body parts, and for providing energy to muscles so they can keep operating.

The most common science fictional explanation for zombie outbreaks is a virus — but viruses and bacterial infections are not known for building large new physical structures within the body. So let’s count viruses out. Instead, the need for a mechanism to activate deteriorating body parts actually provides the cornerstone of what is, in my opinion, the strongest theory: fungal infection.

We know that fungi can infect humans. We also know that fungal networks exist in most of the world’s forests. These mycorrhizal networks have a symbiotic relationship with trees and other plants in the forest, exchanging nutrients for mutual benefit. These networks can be quite large, and there are studies that demonstrate the potential for chemical signals to be transmitted from one plant to another via the mycorrhizal network. That, in turn, means that fungal filaments could perform both vascular and neural functions within a corpse.

This leads us to the following scenario: microscopic spores are inhaled, ingested, or transmitted via zombie bite. The spores are eventually dispersed throughout the body via the bloodstream. Then they lie dormant. When the host dies, chemical signals (or, more accurately, the absence of chemical signals) within the body that occur upon death trigger the spores to activate, and begin growing. The ensuing fungal network carries nutrients to muscles in the absence of respiration or normal metabolism.

Part of the fungal network grows within the brain, where it interfaces with the medulla and cerebellum, as well as parts of the brain involving vision, hearing and possibly scent. Chemicals released by the fungi activate basic responses within these brain areas. The fungi/brain interface is able to convert the electrochemical signals of neurons into chemical signals that can be transmitted along the fungal network that extends through much of the body. This signal method is slow and imperfect, which results in the uncoordinated movements of zombies. And this reliance on the host’s brain accounts for the “headshot” phenomenon, in which grievous wounds to the brain or spine seem to render zombies fully inert.

This leaves the problem of zombie metabolism. Where do the zombies get the nutrients needed to perform physical activity, plus the necessary nutrients to fuel the life-cycle of the fungi? This is most easily explained by the zombies’ constant, endless drive to devour meat. The fungal network would still need some way to metabolize meat, and zombies seem to be able to function even in the absence of a human digestive system.

It is possible that this particular fungi has evolved a means to extract energy and nutrients from meat in a similar manner to carnivorous plants. The ingestion of meat may actually be vestigial, an unintended result of the drive to bite. In this case, the fungi may draw energy from the decomposition of the host’s own organic material, which effectively puts a shelf-life on zombies (in addition to the deterioration of body structures beyond the point where the fungal network can compensate).

Accounts of dismembered parts moving purposefully may be apocryphal.

Now we have established a working theory for fungal zombies. How could such a disease arise? The goal of any biological organism is to live long enough to reproduce, but many pathogens are self-limited by their own lethality. The host dies before it has a chance to spread the pathogen inadvertently. This gives us two pathways for development of the zombie fungus. First, a fungal species existed that used the digestive tracts of mammals to travel. In other words, animals ingested the fungus, including spores. The spores were later defecated out in a new location. Some mutations occurred that caused the spores to gestate while still within the host. However, in most cases, the host’s immune system would destroy the fungus. Further mutations could lead to spores that only trigger once the host has died, avoiding this problem.

Another possibility is a fungal infection that was highly aggressive and caused rapid death within the host. That strain was not able to successfully reproduce as often as a mutated strain that delayed activation until post-mortem.

Of course, it’s one thing for a fungus to activate after the host dies, and quite another for the dead host to stand up and start attacking things. There are many evolutionary steps in between, which is why a zoonotic origin seems likely.

The precursor fungus could have been ingested by pigs, which are omnivorous. Captive pig populations, subject to overcrowding, would have been perfect places for the fungus to spread and mutate. In some poorly managed pig farms, dead pigs may have gone unnoticed, allowing post-mortem development of the fungus. Dead pigs were likely partially eaten by their living counterparts, allowing the fungal strains with post-mortem mutations to spread back into the population. The method of transfer from the pig population to the human population seems fairly obvious.

The evolution of fully mobile dead pigs probably started with a simple bite reflex that could transmit spores to nearby pigs. A bite combined with a muscular spasm, a sort of lunge, would work even better. After many generations, this developed into full post-mortem mobility. Thus, a dead host went from a drawback to an advantage, becoming a mobile platform for spore distribution. In fact, the zombie hunger drive may have originated as a spore distribution method –- only later was the ability to metabolize meat acquired. We can extrapolate this development to assume the further refinement of the fungal neural system, allowing for zombies which are far more coordinated and can run at nearly full speed.

While this type of behavior modification may seem unlikely, there is precedent for it within the animal world. Several species of parasitic wasps are able to reprogram the behavioral patterns of their hosts (bees, ants and even caterpillars), creating complex new behaviors beneficial to the wasp and detrimental to the host. While the hosts in these cases aren’t dead, this does demonstrate that complex chemical overrides can evolve in nature.

Hopefully scientists can develop an effective zombie fungicide in time.