One of the promising areas of research is the investigation into how polyprenols impact Alzheimer's disease. Polyprenols, which are long-chain isoprenoid alcohols of natural origin, are characterized by the general formula H-(C5H8)n-OH, where n represents the number of isoprenoid units. These natural compounds possess strong antioxidant properties and the capacity to enhance brain circulation. They are commonly present in coniferous trees such as cedar, juniper, and fir. Polyprenols play a crucial role in the human body, contributing to various physiological processes such as growth and development, tissue repair, regulation of lipid and carbohydrate metabolism, cellular defense against oxidative stress, and more. Currently, polyprenols are recognized as essential components for the human body.

A recent study clearly demonstrated the hepatoprotective, neuroprotective, and immunomodulatory properties of polyprenols isolated from the green verdure of Picea abies (L.) Karst. This study aimed to investigate effects of polyprenols on oligodendrogenesis, neurogenesis, and myelin content in the cuprizone demyelination model. Demyelination was induced by 0.5% cuprizone solution in CD-1 mice during 10 weeks. Nine cuprizone-treated animals received daily injections of polyprenols intraperitoneally at a dose of 12-mg/kg body weight during Weeks 6-10. Nine control animals and other nine cuprizone-treated received sham oil injections. At Week 10, brain sections were stained for myelin basic protein, neuro-glial antigen-2, and doublecortin to evaluate demyelination, oligodendrogenesis, and neurogenesis. Cuprizone administration caused a decrease in myelin basic protein in the corpus callosum, cortex, hippocampus, and the caudate putamen compared with the controls. Oligodendrogenesis was increased, and neurogenesis in the subventricular zone and the dentate gyrus of the hippocampus was decreased in the cuprizone-treated group compared with the controls. Mice treated with cuprizone and polyprenols did not show significant demyelination and differences in oligodendrogenesis and neurogenesis as compared with the controls.
The results of this study indicate that polyprenols may halt demyelination, restore impaired neurogenesis, and mitigate the reactive overproduction of oligodendrocytes triggered by cuprizone neurotoxicity.

Another preclinical study conducted on rats demonstrated that polyprenols could help regain non-spatial and spatial learning capabilities. In this experiment, beta-amyloid was injected into the fourth ventricle of the rats' brains after surgically opening their skulls. The rats were then orally administered polyprenols.
The outcome of the study revealed a restoration of both non-spatial and spatial learning abilities in the rats. Notably, this study lacked a control group, distinguishing it from the above mentioned research.

Yet another preclinical study, for the first time, assessed the effect of polyprenols on cognitive deficits and neuropathology in mice. At 3 months old, mice were divided into three groups receiving different dosages of polyprenols (low, medium, high) and a drug control group. Age-matched wild-type mice served as the control group. The oral administration of polyprenols lasted for 6 months. The study revealed that polyprenol treatment significantly improved cognitive impairment in double transgenic mice compared to control treatment in behavioral tests. In addition, immunohistochemistry and immunosorbent assays demonstrated a notable decrease in neuritic plaques and hyperphosphorylated tau levels in the brains of mice treated with polyprenols. Furthermore, polyprenol treatment reduced the number of apoptotic cells in brain sections of 9-month-old mice. These findings suggest that polyprenols exert neuroprotective effects in mice and could potentially serve as an effective therapy for various cognitive disorders.

A study conducted in St. Petersburg explored the potential of polyprenols in treating Alzheimer's disease in humans. The research involved 25 patients with an average disease duration of 1.5 years since diagnosis. The treatment course spanned 3-4 months.
The findings revealed that 40% of patients exhibited significant enhancement in cognitive functions, while 48% showed moderate improvements with a reduction in dementia symptoms, transitioning from a severe stage to a milder one. Additionally, 80% of participants experienced improved EEG results during the study.

Based on research findings, polyprenols may have a beneficial impact on the mechanisms underlying the progression of Alzheimer's disease. They can safeguard neurons from oxidative stress, enhance memory and cognitive functions, and reduce brain inflammation. Such properties suggest that polyprenols could potentially slow down the disease progression and enhance the patients' quality of life.
While research in this area is still in its early stages, further clinical trials are necessary to validate the effectiveness of polyprenols in treating Alzheimer's disease. Nonetheless, these substances hold promise as a novel approach in combating this severe illness.
Polyprenols are promising natural compounds that may have a positive effect on Alzheimer's disease. With their antioxidant attributes and capacity to enhance cerebral circulation, polyprenols have the potential to be effective in managing disease advancement and enhancing patient well-being.
However, exploring the full range of polyprenols' properties is challenging due to the extremely high cost of polyprenols of >95% pharmaceutical purity.
Parus Ltd. specializes in producing polyprenols derived from coniferous trees on an industrial scale, making them available in the global market. This enables us to acquire high molecular weight polyprenols while preserving the molecules' stereospecificity at a relatively affordable price.