How 2 Viruses and a Parasite can Lead to Alzheimer’s Disease

Researchers have discovered that the presence of two different virus and a parasite (not all at the same time) can increase a person’s risk for developing Alzheimer’s disease.

All three of them are very common; many millions of people in the US carry at least one of these infections.

And all three usually show no symptoms, and are not problematic for people with healthy immune systems.

But they may be causing damage to your brain.

Read on to discover what they are and what you can do to reduce your risk of developing Alzheimer’s disease.

Continued below…

 

Herpes simplex and Alzheimer’s disease

The human herpesvirus is everywhere. It’s estimated that 65% of adults in the US carry type 1 (HSV-1) herpes, which causes cold sores (or “fever blisters”) around the mouth.

In the US, 20-30% of adults carry herpes simplex type 2 (HSV-2), which is transmitted through sexual contact.

Regarding the virus’s connection to Alzheimer’s disease, a study published in the journal Molecular and Chemical Neuropathology found that people who carry HSV-1 and the apolipoprotein E (apoE) genotype (a known risk factor for Alzheimer’s disease) have a higher risk for developing the neurodegenerative disorder.(1)

Other studies have discovered a relationship between HSV-2 and Alzheimer’s disease as well.(2)

 

Cytomegalovirus

Cytomegalovirus (CMV) is probably the most common virus you’ve never heard of; it’s estimated that 50-80 of every 100 people in the US carry it.

A member of the family of herpesviruses (same as above), CMV lives in body fluids such as saliva and urine, and is spread by close contact.

The signs and symptoms of CMV include fatigue, fever and muscle aches.

In more severe cases CMV can attack specific organs, cause seizures, hepatitis and inflammation of the brain (encephalitis).

And researchers have discovered that exposure to CMV is associated with increased risk of developing Alzheimer’s disease and faster rates of cognitive decline in older adults.(3)

 

A common parasite that can accelerate Alzheimer’s disease

Toxoplasma gondii (TOX) is a parasite that causes toxoplasmosis. It’s estimated 60 million people in the US carry it.

The parasite is transmitted through:

  • Eating–or ingesting raw juices of–undercooked, contaminated meat such as lamb, pork or venison
  • Drinking contaminated water
  • Eating unwashed vegetables grown in soil with the TOX parasite.
  • Coming into contact with cat feces

The presence of TOX in cat feces is why pregnant women aren’t supposed to change litter boxes, because transmission to a fetus can cause serious pregnancy complications.

But that aside, even healthy people with the parasite may be at risk for developing Alzheimer’s disease.

A study performed at Afyon Kocatepe University in Turkey measured TOX antibodies in both healthy people and folks with Alzheimer’s and discovered a positive correlation between the presences of the TOX parasite and the development of Alzheimer’s disease.(4)

 

Chronic infections and Alzheimer’s disease: What’s the connection?

While researchers aren’t sure what it is, exactly, about these viruses that increase the prevalence of Alzheimer’s disease, there’s at least one plausible theory.

Inflammation, as we know, is clearly linked to neurodegeneration and the development of Alzheimer’s and other dementias.

Researchers believe long-term infections, even those that are dormant, cause inflammation in the body and brain, which then weakens the neurons over time.(5)

A study published in the journal CNS Drugs dives deeper into this theory, suggesting viral infections may accelerate neurodegenerative decline by “activating already primed microglial cells within the central nervous system” (CNS).(6)

In plain terms: Microglial cells are the “janitors” of the CNS, and normally only activate when they sense neuronal damage to “sweep away” the affected cells, leaving room for new cells to grow.

But chronic inflammation caused by long-term infection continually activates the microglia, which in turn causes neuronal damage because instead of sweeping away the dead cells, they go haywire and start releasing pro-inflammatory cytokines, small proteins that signal the cells to become even more unstable.(7)

As you can imagine, this causes a chain reaction that, if left unchecked, can quickly lead to neurodegeneration.

Researchers are working on developing anti-inflammatory drugs that will turn off the microglia so that it activates only when necessary.

Until then, the best way to reduce inflammation is, as always, through a nutritious diet of whole foods, plenty of exercise and sleep, and stress management.

 

I don’t want to alarm you with this news. Many millions of people carry these infections without complications. And just because a person has one of these doesn’t mean they will develop Alzheimer’s disease.

In a positive light, these discoveries are good news. We’re getting closer all the time to understanding the genesis of this disease and others like it, which makes us better equipped to fight them.

And that’s something to look forward to.

 

Best Regards,

Lee Euler
Publisher

 

References:

  1. Neurotropic viruses andAlzheimer disease. Interaction of herpes simplex type 1 virus and apolipoprotein E in the etiology of the disease. http://www.ncbi.nlm.nih.gov/pubmed/8871952
  2. Temporal cognitive decline associated with exposure to infectious agents in a population-based, aging cohort. http://journals.lww.com/alzheimerjournal/Abstract/publishahead/Temporal_Cognitive_Decline_Associated_With.99542.aspx
  3. Cytomegalovirus infection and risk of Alzheimer disease in older black and white individuals. http://www.ncbi.nlm.nih.gov/pubmed/25108028
  4. Could Toxoplasma gondii have any role in Alzheimer disease? http://www.ncbi.nlm.nih.gov/pubmed/20921875
  5. A study on the association between infectious burden and Alzheimer’s disease. http://www.ncbi.nlm.nih.gov/pubmed/24910016
  6. Role of infection in the pathogenesis of Alzheimer’s disease. http://link.springer.com/article/10.2165/11310910-000000000-00000
  7. Microglial activation and its implications in the brain diseases. http://www.ncbi.nlm.nih.gov/pubmed/17504139