One in nine Americans aged 65 and older had it Alzheimer’s disease in 2022, and countless others have been indirectly affected as caregivers, healthcare providers and taxpayers.
There is currently no cure – available treatments mainly focus on prevention by promoting and reducing protective factors such as exercise and a healthy diet aggravating factorssuch as diabetes and high blood pressure.
One of these complicating factors is viral infections. Researchers have definitely found that out viruses such as Herpes simplex virus type 1 (HSV-1, which causes cold sores), Varicella zoster virus (VZV, which causes chickenpox and shingles) and SARS-CoV-2 (which causes COVID-19) may lead to an increased risk Alzheimer Illness and dementia after infection.
Figuring out how and when these viruses contribute to disease could help scientists develop new therapies to prevent dementia. But researchers were cannot be recognized permanently suspicious viruses in the brains of people who have died of Alzheimer’s.
Because the process of Alzheimer’s disease can begin decades before symptoms appear, some researchers have suggested this viruses act early”Hit and runThey trigger a cascade of events that lead to dementia but have already started. In other words, by the time researchers analyze patients’ brains, all detectable viral components have disappeared and causality is difficult to establish.
we are a neurovirologist, neurologistand neuroscientist Team interested in the role of viruses in neurodegenerative diseases. In our recently published researchwe are using new technology to look for the tire tracks of these viruses in Alzheimer’s patients.
By focusing on the most vulnerable entry point to the brain, the nose, we uncovered a genetic network that provides evidence for a robust viral response.
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Focus on the olfactory system
Many of the viruses implicated in dementia including herpes viruses and the Virus that causes COVID-19enter the nose and interact with the olfactory system.
the olfactory system is constantly bombarded with smells, pollutants and pathogens. Particles inhaled through the nostrils bind to specific olfactory receptor cells in the tissue lining the nasal cavity.
These receptors send messages to other cells in something called the olfactory bulb, which acts like a relay station that relays those messages down the long nerves of the olfactory tract. These messages are then relayed to the area of the brain responsible for learning and memory, the hippocampus.
The hippocampus plays a crucial role in assigning contextual information to odors, such as B. Danger from the foul smell of propane or comfort from the smell of lavender. This area of the brain is also dramatically damaged in Alzheimer’s disease, leading to devastating learning and memory deficits.
For 85 to 90 percent of Alzheimer’s patients loss of smell is an early sign of disease.
The mechanism leading to the loss of smell in Alzheimer’s disease is relatively unknown.
Like muscles atrophied by lack of use, sensory deprivation It is believed that this leads to atrophy of the brain regions specialized in interpreting sensory information. Strong sensory input to these regions is critical to maintaining overall brain health.
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Odoritis and Alzheimer’s disease
We hypothesize that lifelong viral infections are both contributors and potential drug targets in Alzheimer’s disease. To test this idea, We used new, state-of-the-art technologies to investigate the mRNA and protein networks of the olfactory system in Alzheimer’s patients.
The body uses mRNA, which is transcribed from DNA to translate genetic material into proteins. The body uses certain mRNA sequences to create a network of proteins that are used to fight certain viruses.
In some cases, the body continues activate these pathways even after that virus is eliminated, leading to chronic inflammation and tissue damage. By identifying which mRNA sequences and protein networks are present, we can infer to some extent whether the body has, or has, responded to a viral agent at some point.
So far, sequencing mRNA in tissue samples has been difficult because the molecules are broken down very quickly. However, new technology specifically addresses this issue by measuring small subsections of mRNA simultaneously, rather than attempting to reconstruct the entire mRNA sequence at once.
We used this technology to sequence mRNA from olfactory bulb and olfactory tract samples from six people with familial Alzheimer’s disease, an inherited form of the disease, and six people without Alzheimer’s. We have focused on familial Alzheimer’s disease because the disease is less diverse than the sporadic or non-familial form of the disease, which can result from a number of different individual and environmental factors.
In the familial Alzheimer’s samples, we found altered gene expression that indicates signs of a past viral infection in the olfactory bulb as well as inflammatory immune responses in the olfactory tract. We also found higher levels of proteins involved in demyelination in the olfactory tract of familial Alzheimer’s specimens than in controls.
Myelin is a protective layer of fat around nerves that allows electrical impulses to travel quickly and smoothly from one area of the brain to another. Damage to myelin disrupts signal transmission, leading to impaired neural communication and thus neurodegeneration.
Based on these results, we hypothesize that viral infections and the resulting inflammation and demyelination in the olfactory system may disrupt hippocampal function by impairing olfactory bulb communication. This scenario could contribute to the accelerated neurodegeneration seen in Alzheimer’s disease.
Impact on patient health
Epidemiological data support the role of viral infections in the development of Alzheimer’s disease. For example the Varicella zoster virus is associated with a nearly threefold risk for patients with facial shingles of developing dementia within five years of infection.
A recent report also found a almost 70 percent increased risk for people over 65 to be diagnosed with Alzheimer’s disease within a year of a COVID-19 diagnosis.
These studies suggest that vaccination could be a possible measure to prevent dementia. For example vaccination against seasonal flu virus and herpes zoster is associated with a reduced risk of developing dementia by up to 29 percent and 30 percent respectively.
Further research examining how viral infections can trigger neurodegeneration could help develop antiviral drugs and vaccines against the viruses involved in Alzheimer’s disease.
Andrew BubakAssistant Professor of Neurology, University of Colorado Anschutz Medical Campus; Diego RestrepoProfessor of Cell and Developmental Biology, University of Colorado Anschutz Medical Campusand Maria NagelProfessor of Neurology and Ophthalmology, University of Colorado Anschutz Medical Campus
This article is republished by The conversation under a Creative Commons license. read this original article.
