top of page

About The Vaika Project

Who we are

We are a group of scientists and veterinarians who believe that aging is not an inviolable law of nature, but is rather a condition which can be prevented and/or postponed. This idea is supported by years of our research and we feel that it is time to implement it to practice.

Our non-profit medical research organization is dedicated to extending the health and lifespan of domestic animals. Our company is named in honor of the founders' loyal and beloved friend, a Husky named Vaika.

Learn more about our team

Aged T-cells

Lymphoid cells are responsible for learning and memorizing how to respond to infectious agents. T-cells, in particular, recognize and kill cells that express abnormal antigens—either encoded by infectious agents or mutated genes, which is a hallmark of cells that are on the path to malignant transformation.


However, intrinsic and extrinsic insults that T-cells and their progenitors experience during an organism's life can result in a gradual loss of functionality. As a consequence, aged T-cells have a reduced ability to proliferate in response to antigens.

In our study, we are testing the ability of T-cells to become activated in response to stimulation by measuring the production of cytokines, which are signaling proteins that act as 'immune system hormones.' We use an ELISpot assay to estimate how effectively T-cells can respond to immune stimuli. This and other assays applied to bloodborne T-cells allow us to monitor the decline of their activity with age and assess the effectiveness of our therapy in stopping, slowing down, or reversing this process.

Aged B-cells

B-cells are responsible for production of antibodies recognizing “foreign” (e.g., viral) proteins (antigens) in response to infection. The function of antibodies is to bind the pathogen and inactivate it. In the event of a new infection, naive B cells “learn” to produce antibodies to the antigens of an invader from scratch.


After infection is defeated, most B cells that were recruited to battle with infection die, but a few so-called “memory B cells” stay and can be quickly turned on and start proliferating if the organism meets with the same or similar infectious agent. In healthy young organisms, numerous B cell variants are developed against every new antigen ensuring most effective pathogen inactivation. In an aged organism the repertoire of B cells to any new antigen is much poorer than in a young one and memory B cells are harder to “wake up”. This explains why vaccination is less efficient in the elderly and why they are in general more susceptible to infections.

We are assessing our dogs for susceptibility to immunization. Dogs are regularly vaccinated against leptospirosis, and the titer of antibodies is analyzed. This allows us to track changes in response to vaccination with age, in the presence of anti-aging therapy.

At the time of recruitment to the study, all dogs were tested for the presence of antibodies against infectious diseases in their blood. If it was found that the antibody level is low (or there are none), the dog was vaccinated against the diseases it was not protected from. Anti-Leptosperosis vaccination is done yearly. Prior to the next scheduled treatment, we check the titers of antibodies to reveal whether our anti-aging treatment improves the organism's ability to respond to infectious agents and retain memory of those encounters.

Aged macrophages and neutrophils

"Cleaning of garbage" is one of the immune system's essential functions. This role is played by macrophages and neutrophils, professional cleaners responsible for eradicating cellular pathogens (e.g., bacteria) and remains of dead or broken cells, including both normal and tumor cells.


As macrophages age, they gradually lose their phagocytic abilities. The amount of potentially hazardous objects they can engulf, as well as the speed of this process, decline severely. Increased skin pigmentation in aged people is one of the obvious indicators of this decline. The "impotence" of macrophages contributes to an elevated risk of inflammation, infections, and cancer development with age. We know about this phenomenon mostly from studies done in humans and mice, but it has not been characterized in dogs.

We are collecting macrophages and neutrophils from dogs’ blood at different time points during the duration of our project and check their potential for phagocytosis by “offering” them fluorescent beads resembling type or “garbage” they are made to recognize and engulf. We then use special equipment (fluorescent-activated cell sorter or FACS) to determine how much fluorescent material is inside the cells.


Cytokines are extracellular regulatory proteins that modulate the activity of immune cells. They are a type of hormone of the immune system. Various cell types release them in response to numerous stimuli to trigger immune responses. The ability of a body to release a specific set of cytokines in response to certain stimulation is an important characteristic of the general health status that gets compromised with age.


For example, chronic inflammation, which is a universal hallmark of aging, is associated with an increase in the base levels of a specific set of cytokines in the blood circulation. The release of certain cytokines can be triggered by a rapid change in physiological conditions (e.g., exercise). The scale of this reaction and how soon the cytokine levels come back to a normal state indicate the vulnerability of the organism, which increases with age.

We are checking both steady-state and induced cytokine production following exercise on a treadmill. We are comparing how the rise of cytokine production and the time needed to lower it to a normal state change during the lifetime of our dogs. We are also checking whether the applied treatment could mitigate abnormal reactions that develop with age.

bottom of page