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refers to the relative preservation of neuronal structure
In the case of an ongoing insult (a neurodegenerative insult)
the relative preservation of neuronal integrity implies
a reduction in the rate of neuronal loss over time, which
can be expressed as a differential equation.
It is a widely explored treatment option for many central
nervous system (CNS) disorders including neurodegenerative
brain injury, and spinal
cord injury. Neuroprotection aims to prevent or slow
disease progression and secondary injuries by halting or
at least slowing the loss of neurons.
Despite differences in symptoms or injuries associated with
disorders, many of the mechanisms behind neurodegeneration
are the same. Common mechanisms include increased levels
in oxidative stress, mitochondrial dysfunction, excitotoxicity,
inflammatory changes, iron accumulation, and protein aggregation.
Of these mechanisms, neuroprotective treatments often target
oxidative stress and excitotoxicity—both of which are highly
associated with CNS
disorders. Not only can oxidative stress and excitotoxicity
trigger neuron cell death but when combined they have synergistic
effects that cause even more degradation than on their own.
Thus limiting excitotoxicity and oxidative stress is a very
important aspect of neuroprotection. Common neuroprotective
treatments are glutamate antagonists and antioxidants, which
aim to limit excitotoxicity and oxidative stress respectively.
excitotoxicity is one of the most important mechanisms known
to trigger cell death in CNS
disorders. Over-excitation of glutamate
receptors, specifically NMDA
receptors, allows for an increase in calcium
ion (Ca2+) influx due to the lack of specificity
in the ion channel opened upon glutamate binding.
As Ca2+ accumulates in the neuron, the buffering
levels of mitochondrial Ca2+ sequestration are
exceeded, which has major consequences for the neuron.
Because Ca2+ is a secondary messenger and regulates
a large number of downstream processes, accumulation of
Ca2+ causes improper regulation of these processes,
eventually leading to cell death.
Ca2+ is also thought to trigger neuroinflammation,
a key component in all CNS disorders
antagonists are the primary treatment used to prevent or
help control excitotoxicity in CNS disorders. The goal of
these antagonists is to inhibit the binding of glutamate
receptors such that accumulation of Ca2+
and therefore excitotoxicity can be avoided. Use of glutamate
antagonists presents a huge obstacle in that the treatment
must overcome selectivity such that binding is only inhibited
when excitotoxicity is present. A number of glutamate antagonists
have been explored as options in CNS disorders, but many
are found to lack efficacy or have intolerable side effects.
Glutamate antagonists are a hot topic of research. Below
are some of the treatments that have promising results for
helps regulate excitotoxicity by inhibiting NMDA receptors
as well as other glutamate receptors.
Rd: Results from the study show ginsenoside rd attenuates
glutamate excitotoxicity. Importantly, clinical trials
for the drug in patients with ischemic stroke show it
to be effective as well as noninvasive
Administration of progesterone is well known to aid
in the prevention of secondary injuries in patients
with traumatic brain injury and stroke
Administration in models of Parkinson's disease have
been shown to have pronounced neuroprotective effects
including anti-inflammatory effects due to NMDA receptor
levels of oxidative stress can be caused in part by neuroinflammation,
which is a highly recognized part of cerebral ischemia as
well as many neurodegenerative diseases including Parkinson's
disease, and Amyotrophic
The increased levels of oxidative stress are widely targeted
in neuroprotective treatments because of their role in causing
neuron apoptosis. Oxidative stress can directly cause neuron
cell death or it can trigger a cascade of events that leads
to protein misfolding, proteasomal malfunction, mitochondrial
dysfunction, or glial cell activation.
If one of these events is triggered, further neurodegradation
is caused as each of these events causes neuron cell apoptosis.
By decreasing oxidative stress through neuroprotective treatments,
further neurodegradation can be inhibited.
are the primary treatment used to control oxidative stress
levels. Antioxidants work to eliminate reactive oxygen species,
which are the prime cause of neurodegradation. The effectiveness
of antioxidants in preventing further neurodegradation is
not only disease dependent but can also depend on gender,
ethnicity, and age. Listed below are common antioxidants
shown to be effective in reducing oxidative stress in at
least one neurodegenerative disease:
It targets a diverse array of factors germane to the
pathophysiology of multiple neuropsychiatric disorders
including glutamatergic transmission, the antioxidant
glutathione, neurotrophins, apoptosis, mitochondrial
function, and inflammatory pathways.
Derived from saffron,
crocin has been shown to be a potent neuronal antioxidant.
alpha-estradiol and 17
beta-estradiol have been shown to be effective as
antioxidants. The potential for these drugs is enormous.
17 alpha-estradiol is the nonestrogenic stereoisomer
of 17 beta-estradiol. The effectiveness of 17 alpha-estradiol
is important because it shows that the mechanism is
dependent on the presence of the specific hydroxyl group,
but independent of the activation of estrogen receptors.
This means more antioxidants can be developed with bulky
side chains so that they don't bind to the receptor
but still possess the antioxidant properties.
oil: This contains n-3 polyunsaturated fatty acids
that are known to offset oxidative stress and mitochondrial
dysfunction. It has high potential for being neuroprotective
and many studies are being done looking at the effects
in neurodegenerative diseases
Minocycline is a semi-synthetic tetracycline compound
that is capable of crossing the blood brain barrier.
It is known to be a strong antioxidant and has broad
anti-inflammatory properties. Minocyline has been shown
to have neuroprotective activity in the CNS for Huntington's
disease, Parkinson's disease, Alzheimer's disease, and
Pyrroloquinoline quinone (PQQ) as an antioxidant has
multiple modes of neuroprotection.
Resveratrol prevents oxidative stress by attenuating
hydrogen peroxide-induced cytotoxicity and intracellular
accumulation of ROS. It has been shown to exert protective
effects in multiple neurological disorders including
Alzheimer's disease, Parkinson's disease, multiple sclerosis,
and ALS as well as in cerebral ischemia.
Vinpocetine exerts neuroprotective effects in ischaemia
of the brain through actions on cation channels, glutamate
receptors and other pathways.
The drop in dopamine produced by vinpocetine may contribute
to its protective action from oxidative damage, particularly
in dopamine-rich structures.
Vinpocetine as a unique anti-inflammatory agent may
be beneficial for the treatment of neuroinflammatory
It increases cerebral blood flow and oxygenation.
E: Vitamin E has had varying responses as an antioxidant
depending on the neurodegenerative disease that it is
being treated. It is most effective in Alzheimer's disease
and has been shown to have questionable neuroprotection
effects when treating ALS. Vitamin E ineffective for
neuroprotection in Parkinson's disease.
receptor stimulants can lead to glutamate and calcium
Some other stimulants, in appropriate doses, can however
It has been shown to slow early progression of Parkinson's
disease and delayed the emergence of disability by an
average of nine months.
It has been shown to delay the onset of Parkinson's
disease in studies involving monkeys and humans.
Nicotine is also available as gum.
It is protective against Parkinson's disease.
Caffeine induces neuronal glutathione synthesis by promoting
cysteine uptake, leading to neuroprotection.
neuroprotective treatment options exist that target different
mechanisms of neurodegradation. Continued research is being
done in an effort to find any method effective in preventing
the onset or progression of neurodegenerative diseases or
secondary injuries. These include:
inhibitors: These are primarily used and studied for
their anti apoptotic
factors: The use of trophic factors for neuroprotection
in CNS disorders is being explored, specifically in
ALS. Potentially neuroprotective trophic factors include
aggregation agents: Protein aggregation is a known
source of neuron cell death. Different treatments are
being looked at for potentially eliminating this as
a source of neurodegeneration. These include sodium
4-phenylbutyrate, trehalose, and polyQ-binding peptide.
hypothermia: This is being explored as a neuroprotection
treatment option for patients with traumatic brain injury
and is suspected to help reduce intracranial pressure.
has been reported to protect nerve cells from hypoxia-induced
toxicity (see erythropoietin
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El Toro, 92609,
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Garden Grove, 92840, 92841, 92842, 92843 ,92844, 92845, 92846,
Huntington Beach , 92605, 92615, 92646, 92647, 92648, 92649,
Irvine, 92602, 92603, 92604, 92606, 92612, 92614, 92616, 92617, 92618,
92619, 92620, 92623, 92697,
La Habra, 90631, 90632, 90633,
La Palma, 90623,
Ladera Ranch, 92694,
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Laguna Hills ,92653, 92654,92607,92677,
Laguna Woods, 92637,
Lake Forest, 92630,
Los Alamitos, 90720, 90721,
Midway City, 92655,
Mission Viejo, 92690, 92691, 92692,
Newport Beach , 92658, 92659, 92660, 92661, 92662, 92663, 92657,
Orange, 92856, 92857, 92859, 92862, 92863, 92864, 92865, 92866, 92867,
92868, 92869, Placentia, 92870, 92871,
Rancho Santa Margarita 92688,
San Clemente, 92672, 92673, 92674,
San Juan Capistrano, 92675, 92693,
Santa Ana , 92701, 92702, 92703, 92704, 92705 ,92706, 92707, 92711,
92712, 92725.92735, 92799,
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Sunset Beach 90742,
Trabuco Canyon, 92678, 92679,
Tustin ,92780, 92781,92782,
Villa Park, 92861,
Westminster, 92683, 92684, 92685,
Yorba Linda, 92885, 92886, 92887
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