A shocking new discovery!

Alzheimer’s disease (AD) affects more than 6 million Americans, with the majority of those being 65 and older.

Proteomic analysis of brain tissue from patients diagnosed with Alzheimer’s indicates evidence of fungal proteins.(2) Of those, the most common species were identified as Candida spp., Malassezia spp., Cladosporium spp., and Alternaria spp.(1) These species are all opportunistic microorganisms that infect immunocompromised patients, making Alzheimer’s patients an ideal host. This disease primarily affects those 65 and older due to a weaker immune system, as well as potential changes in diet and hygiene.(3) The question that demands further study is whether or not these fungal infections are the cause of AD. Fungi can lead to a variety of systemic disruptions, including neuroinflammation and neurodegeneration, which can lead to amyloid plaque formation in the brain.

With the disturbances that these fungi present, it is highly possible that chronic fungal infections could be a significant contributor to the degenerative effects of Alzheimer’s disease. A study conducted analyzing brain sections from eleven patients with Alzheimer's - plus three additional control patients, and four patients previously analyzed - found that all the Alzheimer’s patients were infected with fungi, while all the controls were not.(3)

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Fungal elements were found in all the Alzheimer

brains tested, but none in the controls.

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In this study, chitin bodies were found using immunohistochemistry, PCR, and DNA sequencing in the brains of Alzheimer's patients. Chitin is a key component of the fungal cell wall, indicating the possibility that these chitin polysaccharides may originate from fungi. In some cases entire cells of Candida spp were found (shown in photo above). The same study found no fungal elements in the brains of the normal control patients. (3)

Using the same techniques as above, another research group found multiple bacteria and fungi in the brains of Parkinson's patients upon autopsy. Most of the fungal species identified belong to the genera Botrytis, Candida, Fusarium and Malassezia. Some relevant bacterial genera were Streptococcus and Pseudomonas, with most bacterial species belonging to the phyla Actinobacteria and Proteobacteria. (4)

Furthermore, there are other sources of evidence to support the idea that fungi may be contributing to the effects of Alzheimer’s disease, including how the slow progression of the disease fits the nature of untreated fungal infections.(3) These untreated fungal infections can multiply and slowly spread throughout the central nervous system (CNS) eventually leading to the debilitating symptoms observed in Alzheimer’s patients.

Yet another group of researchers found that the common antifungal drug, miconazole, reduced the symptoms of neurodegenerative disease and significantly reduced cognitive impairment in a mouse model; thus, further implicating fungal infections as a cause of AD. (5)

Overall, there is evidence to suggest the presence of fungi found in the brains of Alzheimer’s patients compared to patients without Alzheimer’s. Due to the opportunistic nature of these microorganisms and the compromised immune systems of Alzheimer’s patients, fungi may spread throughout the CNS and contribute to or even cause the adverse symptoms of Alzheimer’s disease.

by Margaux Hanson and Anna Klavins

Technical Services Department, Hardy Diagnostics

Works cited: 1, 2, 3, 4, 5

A gut microbiome imbalance may lead to cancer of the colon

Colorectal cancer (CRC) is the third most common cause of cancer-related death in the United States, with approximately 50,000 deaths reported in 2020. (1) Most cases and deaths may be attributable to risk factors such as age, family history, adenomas, inflammatory bowel disease, or racial and ethnic backgrounds. (2) Other lifestyle-related factors associated to colorectal cancer are weight, smoking, alcohol consumption or diet type. In recent years, increasing importance in the progression of CRC has been linked to the gut microbiome.

Twenty percent of the global cancer burden may be attributed to bacterial pathogens. (3) In colorectal cancer specifically, bacteria associated with carcinogensis, include Helicobacter pylori, enterotoxigenic Bacteroides fragilis, and various pathogenic strains of Escherichia coli. (4) Despite, E. coli being a commensal bacteria in the human microbiota, various studies have demonstrated a relationship between mucosa-adherent E. coli and colorectal cancer. Additionally, several strains of E. coli phylogenic group B2 have been associated with Crohn’s disease, a known risk factor for colorectal cancer. (5) Moreover, mucosa associated or internalized E. coli were observed more often in patients with colorectal cancer than in controls. (6)

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E. coli has been known to damage the DNA of gut epithelial cells

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During the development of cancer, the gut microbiome, immune system, and tumor microbiome may produce an imbalance in bacterial composition (dysbiosis). The tumor microbiome has a negative impact on the gut microbiome causing poor local and systemic responses from host immune system and limited efficacy of chemo- and immunotherapy. When left unchecked in the gut microbiome, pathogenic E. coli can damage the DNA of epithelial cells, i.e., inducing DNA double-strand breaks and/or chromosomal instability (7). The complex immunological cascade that follows could promote the development of an aggressive form of carcinoma.

Predictive and prognostic biomarkers, such as the presence of pathogenic E. coli in stool and the composition of gut microbiomes can be of great use in screening colorectal cancers. There are many interventional approaches to modulating the gut microbiome including pro- and prebiotics, dietary modifications and regular physical activity. It is important to emphasize that by promoting one’s healthy gut microbiome, the overall health of the individual is improved.(8) Until patient-tailored personalized medicine is created, the most effective way to reduce the risk of colorectal cancer is routine screening, beginning at age 45. (9)

by Yesenia Morales

Technical Services Microbiologist, Hardy Diagnostics

References: 1, 2, 3, 4, 5, 6, 7, 8, 9