Why do engineers keep asking me silly questions?

 Maybe because they do not understand the complexity of biological systems.
Or they do not understand that medicine is still an art, where insufficient incomplete information about extremely complex processes
have to be used by Physicians to come to immediate conclusions and decisions.
just for example.
They ask
Why is my depression not improved even after I have taken the medication for more than a week?

 There are approximately 80 billion cells in a human brain.
https://www.nature.com/scitable/blog/brain-metrics/are_there_really_as_many


All we know is that Serotonin and Norepinephrine are important for improving mood.

 among these 80 billion neurons how many are involved in depression is really not known.
 Just for discussion let us say10 billion.
Every single neuron may have thousands of synapses, with chemical signals being passed from axon to dendrite (axodendritic), axon to the soma (axosomatic), or axon to axon (axoaxonic). One type of neuron called the Purkinje cell, found in the cerebellum, may have as many as one hundred thousand synapses.
this is  just about 1/2 a dozen  neurons and  their  connections

Current studies estimate that the average adult male human brain contains approximately 86 billion neurons. As a single neuron has hundreds to thousands of synapses, the estimated number of these functional contacts is much higher, in the trillions (estimated at 0.15 quadrillion).
but we are  dumbing down our discussion so that we can have  something  of  a vague  understanding
so we have to deal with 100,000 X 10 billion synapses.

Some neurobiologists distinguish synapses as Type I and Type II. These synapses vary in size, structure and shape. Type I synapses are found mainly on dendrites and result in an excitatory response in the post-synaptic cell. Type II synapses, in contrast, are found on the soma and inhibit the receiving cell’s activity.
Most synapses are chemical in nature, releasing neurotransmitters or other neuroactive proteins and chemicals to be taken up by receiving cells. Electrical synapses, also known as gap junctions, are smaller, approximately 1-4 nm in width, and conduct impulses in neural circuits that require quick and immediate responses. Additionally, most electrical synapses are bi-directional. Though overlooked for a long time, some now hypothesize that electrical synapses play an equally important role in the creation, maintenance, and strengthening of neural circuits as their chemical brethren.

communicate with one another by releasing small endogenous chemical messengers, called neurotransmitters, into the synapse, where they are then taken up by specific receptors on neighboring cells. There are many types of neurotransmitters in the brain—what they have in common is that they are produced inside a neuron, released into the synapse, and then cause an excitatory or inhibitory effect on receptor cells, helping to propagate or downgrade action potentials.[i] 

Neurotransmitters are often classified into two types: small-molecule transmitters and neuropeptides. Small-molecule transmitters can be further differentiated into monoamines like dopamine and amino acids like glutamate. The neuropeptide class includes endorphins, insulin, and oxytocin. Typically, small-molecule transmitters are direct actors on neighboring cells. Neuropeptides, on the other hand, are better suited for more subtle modulatory effects.[ii]

Originally, neuroscientists believed that each type of neuron released only a single, unique neurotransmitter. This theory, referred to as Dale’s Law or Dale’s Principle after the observations of English neuroscientist Henry Hallett Dale, was first put forward by Australian neurophysiologist and Nobel Laureate John Eccles. Further examination, however, showed that neurons synthesize and release more than one type of neurotransmitter at their terminals. Eccles later revised Dale’s principle to suggest that specific neurons do not release just a single type of neurotransmitter but rather the same set of transmitter types at their synapses.[iii] Today, most neuroscientists posit that most axonal branches of a neuron release the same neurotransmitter(s)—which explains why different neuron types are still referred to as “dopaminergic” or “serotonergic” cells in scientific publications.[iv]

To date, scientists have identified more than 60 different neurotransmitters in the human brain—and expect to find more in the future. They are learning that neurotransmitters like acetylcholine, dopamine, glutamate, serotonin, norepinephrine, GABA, and others play important roles in human cognition and behavior. And while neurotransmitters are too often discussed as having a single role or function, neuroscientists are finding that they are multi-faceted, complex, and interact with one another in a variety of different ways. For example, dopamine has long been thought of as the neurotransmitter involved with reward processing. But new research suggests that the release of acetylcholine results in the release of dopamine—and, ultimately, both influence reward processing and learning.

let us take  just one  neurotransmitter 

Serotonin

Serotonin (5HT), sometimes called the “calming chemical,” is best known for its mood modulating effects. A lack of 5HT has been linked to depression and related neuropsychiatric disorders.[xiii] But 5HT is farther reaching—and has also been implicated in appetite, sleep, memory, and, most recently, decision making behaviors

Serotonin /ˌsɛrəˈtoʊnɪn, ˌsɪərə-/ or 5-hydroxytryptamine (5-HT) is a monoamine neurotransmitter. Biochemically derived from tryptophan,[9] serotonin is primarily found in the gastrointestinal tract (GI tract), blood platelets, and the central nervous system (CNS) of animals, 

Beyo

Binding profile of serotonin
Receptor	Ki(nM)[27]	Receptor function[Note 1]
5-HT1 receptor family signals via Gi/o inhibition of adenylyl cyclase.
5-HT1A	3.17	Memory[vague] (agonists ↓); learning[vague] (agonists ↓); anxiety (agonists ↓); depression (agonists ↓); positive, negative, and cognitive symptoms of schizophrenia (partial agonists ↓); analgesia (agonists ↑); aggression (agonists ↓); dopamine release in the prefrontal cortex (agonists ↑); serotonin release and synthesis (agonists ↓)
5-HT1B	4.32	Vasoconstriction (agonists ↑); aggression (agonists ↓); bone mass (↓). Serotonin autoreceptor.
5-HT1D	5.03	Vasoconstriction (agonists ↑)
5-HT1E	7.53
5-HT1F	10
5-HT2 receptor family signals via Gq activation of phospholipase C.
5-HT2A	11.55	Psychedelia (agonists ↑); depression (agonists & antagonists ↓); anxiety (antagonists ↓); positive and negative symptoms of schizophrenia (antagonists ↓); norepinephrine release from the locus coeruleus (antagonists ↑); glutamate release in the prefrontal cortex (agonists ↑); urinary bladder contractions (agonists ↑)[28]
5-HT2B	8.71	Cardiovascular functioning (agonists increase risk of pulmonary hypertension), empathy (via the spindle neurons or Von Economo neurons[29])
5-HT2C	5.02	Dopamine release into the mesocorticolimbic pathway (agonists ↓); acetylcholine release in the prefrontal cortex (agonists ↑); appetite (agonists ↓); antipsychotic effects (agonists ↑); antidepressant effects (agonists & antagonists ↑)
Other 5-HT receptors
5-HT3	593	Emesis (agonists ↑); anxiolysis (antagonists ↑).
5-HT4	125.89	Movement of food across the GI tract (agonists ↑); memory & learning (agonists ↑); antidepressant effects (agonists ↑). Signalling via Gαs activation of adenylyl cyclase.
5-HT5A	251.2	Memory consolidation.[30] Signals via Gi/o inhibition of adenylyl cyclase.
5-HT6	98.41	Cognition (antagonists ↑); antidepressant effects (agonists & antagonists ↑); anxiogenic effects (antagonists ↑[31]). Gssignalling via activating adenylyl cyclase.
5-HT7	8.11	Cognition (antagonists ↑); antidepressant effects (antagonists ↑). Acts by Gs signalling via activating adenylyl cyclase.

serotonin

Most people associate depression with serotonin-and that, Murrough says, is due to the relatively large success of serotonin-based drugs used to treat the disorder. But while SSRIs work for many people, it's important to remember that depression is not a serotonin disease, says Michael Thase, a psychiatrist at the University of Pennsylvania's Perelman School of Medicine.


 So  it is not  asquare_bsquare.

I may not know the  answer to  that  small  algebra  question  I know more  complex biologic systems  partially.

Binding profile of serotonin
Receptor	Ki(nM)[27]	Receptor function[Note 1]
5-HT1 receptor family signals via Gi/o inhibition of adenylyl cyclase.
5-HT1A	3.17	Memory[vague] (agonists ↓); learning[vague] (agonists ↓); anxiety (agonists ↓); depression (agonists ↓); positive, negative, and cognitive symptoms of schizophrenia (partial agonists ↓); analgesia (agonists ↑); aggression (agonists ↓); dopamine release in the prefrontal cortex (agonists ↑); serotonin release and synthesis (agonists ↓)
5-HT1B	4.32	Vasoconstriction (agonists ↑); aggression (agonists ↓); bone mass (↓). Serotonin autoreceptor.
5-HT1D	5.03	Vasoconstriction (agonists ↑)
5-HT1E	7.53
5-HT1F	10
5-HT2 receptor family signals via Gq activation of phospholipase C.
5-HT2A	11.55	Psychedelia (agonists ↑); depression (agonists & antagonists ↓); anxiety (antagonists ↓); positive and negative symptoms of schizophrenia (antagonists ↓); norepinephrine release from the locus coeruleus (antagonists ↑); glutamate release in the prefrontal cortex (agonists ↑); urinary bladder contractions (agonists ↑)[28]
5-HT2B	8.71	Cardiovascular functioning (agonists increase risk of pulmonary hypertension), empathy (via the spindle neurons or Von Economo neurons[29])
5-HT2C	5.02	Dopamine release into the mesocorticolimbic pathway (agonists ↓); acetylcholine release in the prefrontal cortex (agonists ↑); appetite (agonists ↓); antipsychotic effects (agonists ↑); antidepressant effects (agonists & antagonists ↑)
Other 5-HT receptors
5-HT3	593	Emesis (agonists ↑); anxiolysis (antagonists ↑).
5-HT4	125.89	Movement of food across the GI tract (agonists ↑); memory & learning (agonists ↑); antidepressant effects (agonists ↑). Signalling via Gαs activation of adenylyl cyclase.
5-HT5A	251.2	Memory consolidation.[30] Signals via Gi/o inhibition of adenylyl cyclase.
5-HT6	98.41	Cognition (antagonists ↑); antidepressant effects (agonists & antagonists ↑); anxiogenic effects (antagonists ↑[31]). Gssignalling via activating adenylyl cyclase.
5-HT7	8.11	Cognition (antagonists ↑); antidepressant effects (antagonists ↑). Acts by Gs signalling via activating adenylyl cyclase.

"You don't have a sudden drop in your serotonin when your mood crashes. That's not what is happening," he says. "What's happening, essentially, is a whole system is going offline and we don't know exactly why."

In the past few years, researchers have started to focus more on a different neurotransmitter:  glutamate. This neurotransmitter is essential to learning and memory. "More and more, we're learning that glutamate plays a key role in neuroplasticity and the stress response-and problems with glutamate transmission in the brain may be a bit closer to the fundamental, pathological problem in depression," says Murrough.

Ketamine, better known as an animal tranquilizer, works on a particular receptor in the glutamate system, and studies have suggested it can rapidly reverse depressive symptoms in treatment-resistant patients [See "Ketamine May Help Extinguish Fearful Memories"]. Murrough and colleagues published very positive results on a small clinical trial of ketamine in Biological Psychiatry last year. He says while the work in ketamine is promising, better understanding of abnormalities in the glutamate system may result in even better depression treatments.