Degenerative proteinopathies constitute a set of molecular diseases that are caused by the misfolding of specific proteins, leading them to change their biochemical configuration and become toxic for entire systems of organs. Such protein toxicity induces the lysing of an increasing number of proteins that have a biochemically ‘wild-type’ version, gradually and eventually leading to a complete shift in the ratio between such ‘wild-type’ and ‘altered’ versions of such proteins, which directly precedes the clinical onset of such diseases. Proteinopathies not only involve neurodegenerative illnesses, but also a disease that leads to a progressive rate of blindness. Sadly, all such impairments that are neurodegenerative in nature may only receive palliative treatment, given that they are caused by aggregated proteins that start damaging and destroying entire neuronal systems, which leads to impairments in the neuro-muscular and ultimately to the inability of the patients to perform vital functions, like breathing and deglutition. There is neither a cure, nor a definitive method in which the progression of the illness can be stopped at the present time. Consequently, all neurodegenerative diseases have mortality rates of 100% and clinical approaches aim to reduce the suffering of such patients. Nonetheless, there seems to be a glimmer of hope regarding future prophylactic approaches that could delay the onset of many types of proteinopathies. Namely, an immune application could support efforts of clinical suffering delay and attenuation in an unprecedented manner. At the same time, it is necessary to emphasise upon realistic scenarios, that it remains virtually impossible to delay the onset of proteinopathies to the point of the patient reaching the average number of years in life expectancy without experiencing clinical symptoms yet. Initially, clinicians developed and tested a nasal spray containing a substance known as protollin, which stimulates a restricted extent of adaptive lymphocyte recruitment and transport to the central nervous system areas affected by initial stages of protein aggregation, activating a substantial number of microglial cells and preventing the lysis of numerous astrocytes, which in turn start lysing a number of beta-amyloid protein aggregates together without inducing pathophysiology, given the stage in which the patients have not experienced any clinical manifestation of the neurodegenerative disease yet. In case of an unsuccessful attempt to bring protollin above the threshold levels of clinical safety and efficacy, an immunostimulatory and immunomodulatory substance containing a low concentration of a mixture of recombinant Type I & III Interferons, innate and adaptive lymphocytes, perhaps themselves priorly treated with such IFN glycoproteins, would probably remain a vital candidate for an effective, yet probably still restricted delay of onset of various proteinopathies that could be neurodegenerative and optically degenerative. An existent success rate of the clinical test allows the opening of a window of opportunity regarding an increased efficacy of such adaptive lymphocyte approach, by including recombinant Type I and Type III Interferons into such a nasal spray, which could also enter adaptive lymphocyte and further improve their structural integrity and their multi-lateral functionality. Moreover, a low dose of protollin, Type I Interferons and Type III Interferons could be inserted in combination into adaptive T-Lymphocytes to optimise their defence mechanisms and immune functions, potentially bringing a considerable immunising effect against microbial diseases like HIV-induced, retroviral AIDS. Such an approach could create a stable and wide “highway bridge” of connection between innate and adaptive immunity, aiming for the best version of an immune contribution toward a considerable delay of proteinopathy clinical onset. Overall, there may be a requirement for a bi-lateral update of immunological research covering therapeutics and vaccine development; an immune system based optimisation that builds a stable and wide bridge of connection more directly between pre-cytokine and post-cytokine immune activation, and overall between innate and adaptive immune departments; and a pathogen-based optimisation that either eliminates or partially activates genes suppressive of Type I and Type III Interferon-encoding genes, helping enliven the concept of “United Immune System” as well, though less directly than the immune system-based potential approach.