Updated: Jun 20, 2018
A recent study entitled Microbes and Alzheimer’s Disease (March 2016) conducted by an international team of scientists posits the hypothesis that Alzheimer’s Disease is caused by common microbial infections such as Herpes simplex virus (HSV-1), Herpes simplex encephalitis (HSE), measles (virus), Chlamydia pneumoniae (bacteria responsible for pneumonia), and several types of spirochaete (such as in syphilis), fungal infections and an abnormal microbiota (symbiotic/healthy and pathogenic/unhealthy microbes living inside the human body).
Researchers speculate that microbial infestation specifically enter the brain via the olfactory nerve (leading to the lateral entorhinal cortex from where AD spreads) and/or spread from latent viral presence lodged in the medulla oblongata (brain stem).
A lifetime worth of exposure assures microbial presence (mostly dormant and harmless) in the brain and central nervous system (CNS) of most seniors. While mostly harmless researchers suggest that reactivation may occur after exposure to acute or chronic stress causing a loss of resilience and immunosuppression.
AD is thought to be caused by an accumulation of mal-shaped proteins (tau proteins) along with their precursors (amyloid-β peptides). Amyloid-β peptide is also an antimicrobial (bacteria, fungi, viruses) that increases in the presence of microbial infections. Both are held responsible for loss in nerve and synaptic function. Both are used to diagnose AD. Both have clearly been linked to various microbial presences.
However, while considered the hallmarks of the illness it remains unclear if they are a cause or a result of AD. Either way the authors suggest they are indicators of underlying microbial infections.
The hypothesis posited by the authors of this study demand a deeper examination of the bodies own endocannabinoid system and its effect on AD.
The endocannabinoid system, a system of neuromodulating lipids and their corresponding receptors (CB1 and CB2), are richly present in the brain, spinal cord, and nervous system, including the proposed entry points for the disease, the olfactory bulbs and the brain stem.
Numerous studies have suggested a new and significant role of the endocannabinoid system in the prevention and treatment of AD. Recent findings suggest that even at non-psychoactive dosages activation of CB1 and CB2 receptors via plant-based or man-made cannabinoid molecules realize therapeutic effects in AD such the reduction of β-amyloid peptide and tau build-up.
If we add the well known and positive cannabinoid effects of neuroprotection and capacity for nerve cell repair, the ability to reduce neuroinflammation, the capacity to mitigate mental and emotional stress responses, the antimicrobial effects against MRSA (superbugs aka Methicillin-resistant Staphylococcus aureus), the modulation of mitochondrial dysfunction, and the reduction of oxidative stress, these neuromodulating lipids look to be a very promising potential indeed.
If the author of Microbes and Alzheimer’s Disease are correct that amyloid-β peptide increases in order to fight microbial presence contributes to AD the results from another study conducted at the Shanghai Jiao Tong University School of Medicine (2015)2 offers additional insights and suggestion for a target treatment approach.
Chinese scientists discovered that by suppressing the fatty acid amide hydrolase (FAAH), which breaks down the bodies own, naturally occurring cannabinoid anandamide (actually used was the anandamide analog N-stearoyltyrosine), they were able to offer an effective pharmacological approach to suppress amyloid-β-induced neuropathic injury believed to be the key element in AD.
1 Itzhaki, Ruth F.; Lathe, Richard; Balin, Brian J.; Ball, Melvyn J.; Bearer, Elaine L.; Bullido, Maria J.; Carter, Chris; Clerici, Mario; Cosby, S. Louise; Field, Hugh; Fulop, Tamas; Grassi, Claudio; Griffin, W. Sue T.; Haas, Jürgen; Hudson, Alan P.; Kamer, Angela R.; Kell, Douglas B.; Licastro, Federico; Letenneur, Luc; Lövheim, Hugo; Mancuso, Roberta; Miklossy, Judith; Lagunas, Carola Otth; Palamara, Anna Teresa; Perry, George; Preston, Christopher; Pretorius, Etheresia; Strandberg, Timo; Tabet, Naji; Taylor-Robinson, Simon D.; and Whittum-Hudson, Judith A. Microbes and Alzheimer’s Disease. Journal of Alzheimer’s Disease. Published online March 8 2016 doi:10.3233/JAD-160152
2 Cui H, Yang R, Liu S, Fu G, Lu Y. N-Stearoyltyrosine protects primary cortical neurons against Aβ(1-40)-induced injury through inhibiting endocannabinoid degradation. Life Sci. 2015 Mar 1;124:91-100. doi: 10.1016/j.lfs.2015.01.012.