There has been a worldwide attempt to study SARS-CoV-2 virus for the past three years. The clinical aspects of COVID-19 disease, studies of the virus, and existing knowledge in the area of virology allowed many researchers to make various hypotheses on the underlying mechanisms driving the symptoms of the acute phase and of the long COVID; however, there is no common understanding on what causes these conditions and their treatment modalities. The probable origin of SARS-CoV-2, the fact that it seems to have as a close relative the bat coronavirus RATG13 [1], and that there is a divergence between the two coronaviruses, at least in the region binding domain (RBD) site of the virus major surface protein (spike protein) with the eukaryotic cellular region of the ACE2 receptor [2], do not seem to be enough. It seems that other unknown mechanisms could play a different role in the clinical picture of the neurological manifestations of the patients affected by the acute phase of COVID-19 or by Long COVID. One of the first Chinese studies described the neurological symptoms in a cohort of 214 patients. Of these patients, 36.4% had neurological manifestations, both of the central nervous system (CNS) and peripheral nervous system (PNS). Symptoms reported were dizziness, headache, impaired consciousness, acute cerebrovascular disease, ataxia, seizures, altered taste and smell, vision problems, nerve pain, and skeletal muscle injury [3]. In addition to this finding, another review also reports cerebral venous (sinus) thrombosis, epilepsy, meningitis, encephalitis, meningoencephalitis, Gullain–Barrè syndrome (GBS), Miller Fisher syndrome (MFS), acute myelitis and reversible posterior encephalopathy syndrome (PRES) [4,5]. Furthermore, in children, even if the current literature reports a low manifestation of the severe acute phase, it is possible to observe important neurological symptoms [6]. Regarding long COVID conditions, Premraj et al. [7] reported a statistical analysis of 1458 articles. The prevalence of post-COVID-19 neurological symptoms were observed: fatigue, brain fog, memory issues, attention disorder, myalgia, anosmia, dysgeusia, and headache, while neuropsychiatric conditions observed are sleep disturbances, anxiety, and depression. Some neurological symptoms such as anosmia or dysgeusia, or others are not only present in COVID-19 patients but are also described in other diseases like Parkinson’s (PD) [8,9] or Alzheimer’s (AD) [10]. It is noted that one important pathway implicated in these neurological disorders is the cholinergic system [11], and a possible role of this mechanism has also been observed in COVID-19 patients [12,13,14], and some authors have observed a decrease in Butyrylcholinesterase (BChE, BuChE), a pseudocholinesterase, implicated in the hydrolysis of many different choline-based esters, along with Acetylcholinesterase (AChE), in COVID-19 patients [15,16]. These authors [16] observed how the outcome of hospitalized cases correlated with low levels of these enzymes. They also observed how there is a correlation between these enzyme levels and the C-reactive protein (PCR) of the patients. It should be considered that these enzymes, AChE and BChE, are known in the literature to be important in choline reuptake and acetylcholine sequestration and degradation. The parasympathetic system is involved in the pathology of COVID-19, and the clinic described increasingly indicates its marked connection with the cholinergic system [12,13,14]. These mechanisms are similar to those observed in the clinical of toxicological manifestation [17,18]. Depending on the metabolites or toxicological peptides, an agonist effect on nicotinic and muscarinic receptors or saturation of AChE and BChE enzymes can be observed, resulting in hyperactivation of cholinergic signaling or blockade [17,18]. On the other hand, many papers show the connection between PD [19,20] or AD [20,21], and the gut microbiome. They observed how the microbiota and the composition of the bacterial population change in these diseases, in contrast to the healthy population. In general, it has been noted that bacteria produce toxins [22,23], and with regard to other coronavirus it has been observed that host cells can produce peptides able to inhibit the binding between viral particles such as the Spike (S) protein and the infected cell’s surface, and that the mechanism of action appears to interfere with its folding and prevent entry [24,25]. At the same time, a category of compounds better defined as antimicrobial peptides (AMPs) is known to be present in nature and to have antiviral properties [26,27]. They are usually cationic peptide molecules (in the range 10–60 amino acids) secreted to contrast microbes (bacteria, fungi, small parasites or viruses), but examples of anionic ones, due to abundance of aspartic and glutamic amino acids, have been reported as well [26]. AMPs can be produced by eukaryotic cells such as mammalian and insect ones (they are called “defense oligopeptides” [27]), but also by microorganisms such as bacteria [27]. Some AMPs show specific antiviral action, such as those against human immunodeficiency virus (HIV). Examples of collections of natural antimicrobial peptides are also available, such as the antimicrobial peptide database 3 (APD3) [28]. AMPs with antiviral action usually show a mechanism able to prevent viruses from binding to cells or interfering with viral replication mechanisms [29]. Observations show that AMPs against viruses [30] can be diversified into peptides derived from the heptad repeat 1 (HR1), heptad repeat 2 (HR2), or region binding domain (RBD) subunits of the spike protein [31]. These peptides can also be derived from other AMP peptides or derived from nonstructural proteins [31].