This is the finding of a new study conducted by
researchers from the University of California-
Riverside (UC-Riverside), recently published in
PLOS Pathogens .
T. gondii is a single-celled parasite that can
cause a disease known as toxoplasmosis.
Infection with the parasite most commonly
occurs through eating undercooked,
contaminated meat or drinking contaminated
water.
It may also occur through accidentally
swallowing the parasite after coming into
contact with cat feces - by cleaning a litter tray,
for example.
Though more than 60 million people in the United
States are believed to be infected with T. gondii ,
few people become ill from it; a healthy immune
system can normally stave it off.
As such, most people who become infected with
the parasite are unaware of it.
Those who do become ill from T. gondii infection
may experience flu-like symptoms - such as
swollen lymph glands or muscle aches - that last
for at least a month.
In severe cases, toxoplasmosis can cause
damage to the eyes, brain, and other organs,
though such complications usually only arise in
people with weakened immune systems.
The new study, however, suggests there may be
another dark side to T. gondii infection: it may
lead to development of neurodegenerative
disease in people who are predisposed to it.
To reach their findings, lead author Emma Wilson
- an associate professor in the Division of
Biomedical Sciences at the UC-Riverside School
of Medicine - and colleagues focused on how T.
gondii infection in mice affects glutamate
production.
How a build- up of glutamate can damage
the brain
Glutamate is an amino acid released by nerve
cells, or neurons. It is one of the brain's most
abundant excitatory neurotransmitters, aiding
communication between neurons.
However, previous studies have shown that too
much glutamate may cause harm; a build-up of
glutamate is often found in individuals with
traumatic brain injury (TBI) and people with
certain neurodegenerative diseases, such as
multiple sclerosis (MS) and amyotrophic lateral
sclerosis (ALS).
The researchers explain that excess glutamate
accumulates outside of neurons, and this build-
up is regulated by astrocytes - cells in the
central nervous system (CNS).
Astrocytes use a glutamate transporter called
GLT-1 in an attempt to remove excess glutamate
from outside of neurons and convert it into a
less harmful substance called glutamine, which
cells use for energy.
"When a neuron fires, it releases glutamate into
the space between itself and a nearby neuron,"
explains Wilson. "The nearby neuron detects this
glutamate, which triggers a firing of the neuron.
If the glutamate isn't cleared by GLT-1 then the
neurons can't fire properly the next time and
they start to die."
T . gondii increases glutamate by inhibiting
GLT- 1
In mice infected with T. gondii , the researchers
identified an increase in glutamate levels .
They found that the parasite causes astrocytes
to swell, which impairs their ability to regulate
glutamate accumulation outside of neurons.
Furthermore, the parasite prevents GLT-1 from
being properly expressed, which causes an
accumulation of glutamate and misfiring of
neurons. This may lead to neuronal death, and
ultimately, neurodegenerative disease.
Source: medicalnewstoday.com
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