Neuroprotective effects of vitamins C and E against epilepsy-induced neuronal death

Epilepsy is thought to be associated with oxidative stress, which play its role in the seizures-induced neuronal death (1, 2). On the other hand, the brain, due to a high content of polyunsaturated fatty acids, is an easy target for the peroxidation. Luckily, it has neuroprotective systems such as superoxide dismutase, catalase, glutathione peroxidase and reduced glutathione (3, 4).

Exogenous antioxidants like vitamin E and C, can inhibit the neuronal damage provoced by lipid peroxidation during seizures and prevent the increase in brain free fatty acid levels, suggesting that the protection may be mediated by, for example, increase of hippocampal catalase activity (5). Vitamin C significantly decreased the lipid peroxidation after seizures induced by cholinergic agonist pilocarpine supporting the idea of interaction of the C and E vitamins with catalase activity to produce neuronal protection amd to decrease the lipid peroxidation level (6).

When oxidative damage accumulates over  years, it may account for the increased incidence of neurodegenerative diseases in aged populations. The mechanisms of neuronal degeneration in these cases remain unknown and this is a major obstacle in the development of effective therapies targeting the causes of the diseases.

Sources

  1. Neurosci Lett 420 (2007), pp. 76–79
  2. Neurosci Lett 291 (2000), pp. 179–182
  3. Cell signaling and neurotoxic events. In: L.W. Chang, Editor, Principles of Neurotoxicology, Marcel Dekker, New York (1994), pp. 475–493
  4. Neurosci Lett 8 (2007), pp. 76–79
  5. Epilepsy Res 46 (2001), pp. 121–128
  6. Pharmac Biochem & Behavior, Volume 89, Issue 1, March 2008, Pages 1-5

Music is good for the brain

The study conducted by researchers at McGill University in Montreal and published in January 2011 issue of Nature Neuroscience showed that the music increased dopamine levels in certain areas of the brain. Various types of music were shown to be effective depending on individual preferences. (1). On the other hand, dopamine is crucial in the brain system of movement organization, deficiencies of brain cells producing dopamine, as we know, result in Parkinson’s disease, and the only reliable method of treatment is the L-DOPA medication having severe side effects and gradually losing its efficiency as the disease progresses.

Other studies revealed that music (e.g., exposure to Mozart’s music) can decrease the blood pressure in hypertensive patients and even experimental animals. Increased dopamine levels improve dopaminergic neurotransmission in epilepsy (2), dementia (3), and ADHD (4).

The beneficial effects of music are thought to work through brain structures involved in reward processing including the nucleus accumbens* and the ventral tegmental area**, hypothalamus*** and insula****

Sources

1. Music – it does a body and mind good, Baxterbulletin.com

2. Brain Res. Rev. 25 (1997), pp. 1–26

3. Exp. Aging Res., Volume 27, Issue 3 July 2001 , pp. 215 – 228

4. J. Learn. Disabil. 29 (1996), pp. 238–246

Footnotes

* also known as “center of motivation”

** a component of the reward pathway in the brain

*** a very important brain area responsible for many bodily functions as well as instincts for basic survival, fight or flight, mating, eating, and drinking, etc.

**** linked to emotions, perception, motor control, self-awareness, cognitive functioning, and interpersonal experience.

Energy substrates and neuroprotection: what does what

A few interesting articles about glucose, lactate, and pyruvate
and their neuroprotective functions.

J Neurochem. 2010 Feb 15
Chronic in vitro ketosis is neuroprotective but not anticonvulsant.
Marina Samoilova, Michael Weisspapir, Peter Abdelmalik, Alexander A
Velumian, Peter L Carlen

Chronic in vitro treatment with a ketone body, D-beta-hydroxybutyrate
(DbetaHB), protected the cultures against chronic hypoglycemia,
oxygen-glucose deprivation and NMDA-induced excitotoxicity, but failed
to suppress intrinsic and induced seizure-like activity, indicating
improved neuroprotection is not directly translated into seizure
control. However, chronic in vitro ketosis abolished hippocampal
network hyperexcitability following a metabolic insult, hypoxia,
demonstrating for the first time a direct link between metabolic
resistance and better control of excessive, synchronous, abnormal
electrical activity.

Neuroscience. 2007 Jun 7
Lactate, not pyruvate, is neuronal aerobic glycolysis end product: An
in vitro electrophysiological study. A Schurr, R S Payne

We hypothesized that, in the brain, both aerobic and anaerobic
glycolysis terminate with the formation of lactate from pyruvate by the
enzyme lactate dehydrogenase (LDH). If this hypothesis is correct,
lactate must be the mitochondrial substrate for oxidative energy
metabolism via its oxidation to pyruvate, plausibly by a mitochondrial
LDH

Neurosci Res. 2004 Dec;50 (4):467-74
Glycolysis regulates the induction of lactate utilization for synaptic
potentials after hypoxia in the granule cell of guinea pig hippocampus.
Toshihiro Takata, Bo Yang, Takashi Sakurai, Yasuhiro Okada, Koichi
Yokono

Population spikes are not maintained with lactate following hypoxia in
10 mM glucose medium, but are maintained at their original levels with
lactate after exposure to hypoxia in lower concentration (5 mM) of
glucose.

Neurosci Res. 2003 Jul ;46 (3):333-7
Effects of lactate/pyruvate on synaptic plasticity in the hippocampal
dentate gyrus.
Bo Yang, Takashi Sakurai, Toshihiro Takata, Koichi Yokono

Replacement of glucose with lactate and pyruvate maintained population
spikes after transient depression, and supported a similar degree of
paired-pulse facilitation. These results indicate that monocarboxylates
could serve as sufficient substrates LTP but with less efficiency than
glucose.

Neuroscience. 2007 Jun 7
Lactate, not pyruvate, is neuronal aerobic glycolysis end product: An
in vitro electrophysiological study.A Schurr, R S Payne

 

We hypothesized that, in the brain, both aerobic and anaerobic
glycolysis terminate with the formation of lactate from pyruvate by the
enzyme lactate dehydrogenase (LDH). If this hypothesis is correct,
lactate must be the mitochondrial substrate for oxidative energy
metabolism via its oxidation to pyruvate, plausibly by a mitochondrial
LDH


Neurosci Res. 2004 Dec 50 (4):467-74
Glycolysis regulates the induction of lactate utilization for synaptic
potentials after hypoxia in the granule cell of guinea pig
hippocampus.Toshihiro Takata, Bo Yang, Takashi Sakurai, Yasuhiro Okada,
Koichi Yokono

 

Population spikes are not maintained with lactate following hypoxia in
10 mM glucose medium, but are maintained at their original levels with
lactate after exposure to hypoxia in lower concentration (5 mM) of
glucose.

 

A serious reason to avoid energy drinks: they can cause seizures

Epilepsy,Miscellaneous — 12:16 pm

Energy drinks usually contain a lot of of caffeine, sugar, usually taurine [used to prevent oxidative stress induced by exercise 30, and to enhance weight loss (2) and to reduce anxiety levels, (3)], B-vitamins, ginseng, inositol [preliminary results exist that it can be effective in treating depression, and panic attacks, (4)], an anti-oxidant carnitine, and Guarana, rich in caffein. (more…)

Not only ketone bodies: on neuroprotective effects of energy substrates

In the previous post On the mechanisms of brain protection by ketones, I described how a shortage of ketones caused pathological changes in brain cells in brain slices (in vitro, 1) and in whole animals (in vivo, 2) resulting in abnormal (excitatory) behavior of GABA, the principal brain chemical helping to resist hyperactivity. (more…)

Ketogenic diet efficiency in experiments and clinical trials

 

See References in this post

 
Ketogenic diet efficiency has been studied for different age groups, species, types of diet including LCT and MCT triglycerides or types of fatty acids, calorie restriction, glycolysis limitation, etc.

Ketogenic diet efficiency in experiments and clinical trials

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