Age-related cognitive diseases

Neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease, dementia, and others, are incurable, terminal illnesses that are characterized by progressive neurodegeneration and cognitive decline. These age-dependent cognitive disorders are major debilitating events that affect the lives of millions of individuals after age 60. Indeed, greater than 30 million people currently suffer from Alzheimer’s disease within the US, and the number of patients is predicted to double every 20 years unless preventive measures are developed.
Meanwhile, approximately 60,000 new cases of Parkinson’s disease are diagnosed annually in the US, and the disease is expected to afflict more than 10 million citizens within the next 15 years.

HMI scientists have discovered and are intensively studying new paradigms regarding the role of the microbiome in triggering and promoting these cognitive diseases. Indeed, our research will enable amazing advances in our understating of the mechanisms by which these organisms affect human aging-related cognitive decline.

The HMI is utilizing microbiological, biochemical, mathematical, genetic, and molecular tools to understand how age-related diseases, including neurodegenerative disorders, are affected by particularities in host-microbiota cross-talk, and to successfully identify new ways of preventing and managing these diseases in humans.


Novel Pathogens Research

The HMI is focused on understanding how previously uncharacterized infectious agents within the microbiota might trigger the onset and progression of Alzheimer’s disease, Parkinson’s disease, and dementia. Using unique methods developed by HMI scientists, our search for novel pathogens and subsequent evaluation of their role in human disease, as well as our analyses of the particularities of human-microbiota cross-talk, is opening up new possibilities for understanding the pathogenesis of neurodegenerative diseases, and may facilitate the development of methods for the prevention and treatment of these disorders, and give rise to a system for personalized microbiota care.

Novel Therapeutic Directions


The HMI is currently developing a unique product that is based on unanticipated results obtained from a study of distinct mechanisms of cooperation between the microbiota and mitochondria, named “HMI-M- Transplantat”. This therapeutic solution for the first time takes into consideration the unexpected link between the microbiota and the host organism, and is based on the Tetz Theory of longevity, maternal inheritance of microbiota, diseases of the microbiota, and the Pangenome concept. Moreover, the IHM is developing individualized algorithms for the usage of this unique product to prevent and overcome age-related cognitive diseases.

The IHM has discovered a novel compound that exhibits multipotent targeting of factors involved in macroorganism-microbiota cross-talk. Using this new therapeutic compound, we may be able to influence cognitive diseases.

Our research, based on theories developed here at the HMI, has revealed entirely new aspects of the biology of age-related cognitive diseases, and has identified a new group of potential therapeutic targets. By targeting these factors, it may be possible to reduce the severity of clinical symptoms associated with Alzheimer’s disease, Parkinson’s disease, and dementia. Moreover, our findings have resulted in the development of a first-in- class, potentially groundbreaking, therapeutic solution named NT-49, which is currently under intensive study at the HMI.

The Human Microbiology Institute is dedicated to collaborate with other research organizations and entities involved in this field. To that end the HMI will develop means by which to make the results of this research widely available on a non-discriminatory basis.


We try to make our data available to the whole scientific community. The IHM welcomes collaborative studies to unravel the pathogenesis of human diseases associated with the microbiota. However, we ask that you respect the rights of first publication and cite our work as follows:

Effect of deoxyribonuclease I treatment for dementia in end-stage Alzheimer’s disease: a case report.