Sweet and sour recipes for the brain. 3. Let the neurons breathe!

Brain metabolism,Energy Substrates,Methodology — 2:30 pm

Latest update: Critical State of Energy Metabolism in Brain Slices: The Principal Role of Oxygen Delivery and Energy Substrates in Shaping Neuronal Activity 

Part 2. Energy substrates: too sour?
Part 3. Let the neurons breathe!

In the recent experimental work by Ivanov et al., the authors discuss (among other things) the role of oxygenation in neuronal efficiency. They cite the works showing that in adult animals, both synaptic function and neuronal networking strongly depend on the level of oxygenation in brain slices. They further registered the oxygenation levels at various speed of brain slice’s perfusion with artificial cerebrospinal fluid (ACSF, read more about it – > here) in very young animals. They showed that in a standard camera (importantly: as opposite to the interface cameras) at an upper-standard perfusion rate of 3.25 ml/min oxygen content is only 50% of that showed in their experiments with the flow rate of 9 ml/min, and that’s on the slice’s surface. Deeper into the slice’s tissue, oxygenation rapidly decreased and in the middle of a 400 micron-thick slice, oxygen is completely absent. A decrease in the perfusion rate from 15 ml/min to 3.25 ml/min resulted in an about two-fold reduction of the amplitude of so called local field potential (a measure of synaptic robustness). They concluded: “Therefore, as in more mature neurons (Schurr and Payne, 2007; Hajos et al., 2009; Garcia et al., 2010), the synaptic function of neonatal neurons during network activity profoundly depends on oxidative metabolism.”

Interestingly, the authors who failed reproducing some of the effects of energy substrates shown by the group of Y. Zilberter in 2009-2011 used the experimental design corresponding to a severe lack of oxygen in slices.

Thus, Tyzio et al., 2011, in their imaging experiments worked with neuronal populations occupying in slices deeper areas than those in which oxygen can be supplied at the used perfusion rate 2–3 ml/min. Same is true for the work of Ruusuvuori et al., 2010 since they registered GDPs that also involves neuronal populations larger than the oxygenation areas in the slices.

This is an important difference in experimental techniques used by the above mentioned authors on one hand and: Rheims et al., 2009, Holmgren et al., 2010, Mukhtarov et al., 2011, Ivanov et al., 2011 on the other hand – where the perfusion rates of 9 to 15 ml/min were used.

This alone can explain the difference in effects of one of the ketone bodies observed by Holmgren et. al., 2010 and Tyzio et al., 2011. The matter is, for BHB to act, oxygen availability is mandatory while glucose can work in anaerobic condition although in this case, it yields much less energy: 2 molecules of ATP for each molecule of glucose comparing with 32 molecules of ATP for each molecule of glucose in aerobic conditions (Lehninger, 2005). No wonder anaerobic glycolysis, especially in very young animals, fails supporting normal neuronal activity. A vicious circle may occur: lack of energy -> neuronal hyperactivity -> increased energy demand -> increased energy deficit, etc.

References

  1. Garcia, A.J., 3rd, Putnam, R.W., and Dean, J.B. (2010). Hyperbaric hyperoxia and normobaric reoxygenation increase excitability and activate oxygen-induced potentiation in CA1 hippocampal neurons. J Appl Physiol 109, 804-819.
  2. Hajos, N., Ellender, T.J., Zemankovics, R., Mann, E.O., Exley, R., Cragg, S.J., Freund, T.F., and Paulsen, O. (2009). Maintaining network activity in submerged hippocampal slices: importance of oxygen supply. Eur J Neurosci 29, 319-327.
  3. Holmgren CD, Mukhtarov M, Malkov AE, Popova IY, Bregestovski P, Zilberter Y (2010) Energy substrate availability as a determinant of neuronal resting potential,GABAsignaling and spontaneous network activity in the neonatal cortex in vitro. J Neurochem 112:900 –912.
  4. Ivanov A, Mukhtarov M, Bregestovski P and Zilberter Y (2011). Lactate effectively covers energy demands during neuronal network activity in neonatal hippocampal slices. Front. Neuroenerg. 3:2.
  5. Khakhalin A (May 18, 2011). Questioning the depolarizing effects of GABA during early brain development. <a style=”color: #cc0000;” title=”Questioning the depolarizing effects of GABA during early brain development” href=”http://jn.physiology.org/content/early/2011/05/13/jn.00293.2011.abstract” target=”_blank”>J Neurophysiol doi:10.1152/jn.00293.2011</a>.</p>
  6. Ruusuvuori E, Kirilkin I, Pandya N, Kaila K. Spontaneous Network Events Driven by Depolarizing GABA Action in Neonatal Hippocampal Slices are Not Attributable to Deficient Mitochondrial Energy Metabolism. J Neurosci. 2010 Nov 17;30(46)
  7. Lehninger, A.L. (2005). “Oxydative phosphorylation and photophosphorylation,” in Principles of biochemistry, eds. D.L. Nelson &amp; M.M. Cox. Forth ed: W. H. Freeman), 690-740.
  8. Schurr, A., and Payne, R.S. (2007). Lactate, not pyruvate, is neuronal aerobic glycolysis end product: an in vitro electrophysiological study. Neuroscience 147, 613-619.
  9. Tyzio, R., Allene, C., Nardou, R., Picardo, M.A., Yamamoto, S., Sivakumaran, S., Caiati, M.D., Rheims, S., Minlebaev, M., Milh, M., Ferre, P., Khazipov, R., Romette, J.L., Lorquin, J., Cossart, R., Khalilov, I., Nehlig, A., Cherubini, E., and Ben-Ari, Y. (2011). Depolarizing actions of GABA in immature neurons depend neither on ketone bodies nor on pyruvate. J Neurosci 31, 34-45.

The basics of ketogenic diet: works of Shaffer and Wilder & Winter

Glucose,Ketogenic diet,Ketone bodies,Ketosis, ketogenesis,Methodology — Tags: , — 6:16 am

It is interesting that while the ketogenic diet becomes well researched as a method for improving energy metabolism during quite a few medical conditions and the number of original research articles as well as reviews grow currently approaching 15,000, only 19 out of all of them cite the original work, which in fact is the basis of the diet. >>> Read more

The ketogenic diet is no longer considered a strictly anti-epileptic diet: its suggested and tested applications includes a broad spectrum of disorders of energy metabolism. The ketogenic ratio formula used in clinics for calculating the ketogenic diet composition was offered by Wilder and Winter in 1922 (1). They argued that the levels of ketogenic substances depend on the ratio between fatty acids and glucose of the metabolizing foods. The ratio when ketogenesis is initiated they called the threshold of ketogenesis: “When the proportion of acetoacetic acid to glucose in such mixtures was that of 1 (or possibly 2) molecules of acetoacetic acid to 1 of glucose, the former substance was completely oxidized. When the proportion of glucose was less, a considerable fraction of acetoacetic acid escaped oxidation.”

Shaffer (2, 3) calculated the number of molecules of ketogenic substrates corresponding to the number of molecules of glucose and concluded that the maximal ratio compatible with the oxidation of the ketogeniec compounds was reached when a ratio of of ketogenic molecules to the number of glucose molecules was 1: 1. He subsequently considered that each glucose molecule is ketolytic for 2 molecules of acetoacetic acid, a 2:l ratio.

Wilder and Winter, 1922 included in their formula the following measurements obtained in clinical settings:

1) basal metabolism for 24 hour periods plus 10 per cent for the specific dynamic action of food and 10 per cent for movements;

2) the calories from the protein metabolism assessed by nitrogen excretion;

3) the calories from fat metabolism taken as the sum of the calories of protein and carbohydrate combined subtracted from the total calories of the day.

The values for carbohydrate and fat are used in the calculation of the ratio between the ketogenic molecules and the glucose molecules (2, 3).

“Under the conditions of these experiments, provided these assumptions are tenable, the ratio between the ketogenic and the glucose molecules at which a clinically significant ketosis appears has a value of at least 2: 1. A ratio of this value implies that every molecule of glucose is ketolytic for 2 molecules of acetoacetic acid.”

References

  1. Wilder R., Winter M. Thew threshold of ketogenesis. J. Biol. Chem. 1922 52: 393-401.
  2. Shaffer, P. A., Antiketogenesis. I. An in vitro analogy, J. Biol.Chem., 1921, xlvii, 433.
  3. Shaffer, P. A., Antiketogenesis. II. The ketogenic antiketogenic balance in man, J. Biol. Chem., 1921, xlvii, 449.

 

 

 

Alzheimer’s disease and a long-standing exposure to glucose in the Western diet

Alzheimer's,Glucose,Ketone bodies,Lactate — 6:35 am

 

Chronic exposure to glucose due to the traditional Western diet impairs neuronal function and causes apoptosis (programmed neuronal death), concluded Drs Seneff & Wainwright (UK) and Mascitelli (Italy). Their reasoning was roughly the following:

The amyloid-beta peptide (AB) in Alzheimer’s disease (AD) plaques so far seen as a hallmark of this disease, in fact may be an early attempt of protection from its development.  AB switches neuronal metabolism from glycolysis-based to the use of other substrates, e.g., lactate and ketone bodies. This is a very important adjustment in the AD case since there’s an insulin resistance in the AD brain indicating an inadequate ability to utilize glucose. Moreover, the levels of advanced glycation end-products (harmful in any case) are increased in AD. The damage they induce interferes with delivery of fats and cholesterol to astrocytes, and consequently to neurons. This is important because for smooth communication between neurons, sufficient levels of fat and cholesterol is required and the AD CSF is deficient in both. Synthesis of AB is increased when lipid supply is deficient. In the condition of this deficiency, there’s an increase in synthesis of excitatory neurotransmitter glutamate leading to oxidative damage and toxic overexcitability.

The good news is, wrote the authors, a simple dietary change towards lower carbohydrate intake and higher fats intake, may be efficiently protective against AD.

Source:

European Journal of Internal Medicine 22 (2011) 134–140

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

Epilepsy,Neuroprotectors — Tags: , , , , — 7:49 am

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

Toxic glycolysis and brain aging

Glucose,Hormesis,Theories — Tags: , , , , , , — 8:29 am

Related article: Prescription-strength stress as a medicine

The intermittent glycolysis during fasting, physical exercise, and stress may delay senescence by lowering intracellular concentration of methylglyoxal, a common intermediate in the Maillard reaction (glycation).

A simple logic allows to imagine that a situation when food is available to an animal at all times and in any quantities should be very seldom. In real life, there are seasons when food is abundant and seasons when it’s scarce. To smoothen the energy delivery to vital organs, there all kind of depots, most famous (or rather infamous for us human beings in Western societies) is the fat depot, having practically unlimited capacity. There is clinical evidence that a human body can save in this depot enough energy to feed itself for a year. Vitamins and electrolyte fluids should be adequately supplied of course, but no calories enter the body – and it survives!

The opposite situation, when animals are allowed to eat as much as they can, as often as they can, is called ad libitum (AL). In experiments on beneficial effects of calorie restriction (CR), the food intake in the AL situation is taken for 100% and then different percentages of restrictions are applied to see CR effectiveness to slow down the process of aging, especially brain aging.

In an early study of the energy metabolism McCarter and Palmer (1) interesting differences were revealed, between rats fed CR diets and those fed the same food but AL. Although in both groups energy metabolism was mostly glycolytic, taping in carbohydrate metabolic way, CR very soon after feeding switched to using their bodies’ fat reserves with their glycolysis suppressed, while the AL group maintained practically non-stop glycolysis.

So it’s been suggested that that the beneficial effects of CR could be due to suppression of glycolysis and in experiments of Walker et al. (2) and Partridge and Brand (3) the question of whether the shortened life-span of AL animals results from some metabolic toxicity, specifically whether glycolysis is deleterious but possibly hormetic (4)

The hormesis hypotheses by Masoro (5) and Sinclair (6) suggests that intermittent stress may induce synthesis of long-term protective functions. Glycolytic intermediates dihydroxyacetone- and glyceraldehyde-3-phosphates are form methylglyoxal (MG), which is potentially toxic.

Hipkiss (7) suggested that non-stop glycolysis is deleterious due to the generation of MG, but periods of glycolysis interruption could be hormetic. MG damages mitochondria and induces a pro-oxidant state characteristics to cellular aging. The decreased glycolysis during CR may delay senescence by lowering intracellular MG concentration compared to AL animals.

Sources

1. Am. J. Physiol. 1992 263, E448-E452

2. Mech. Ageing Dev. 2005 126, 929-937

3. Mech. Ageing Dev. 2005 126, 911-912

4. Hormesis – An effect in which a toxic substance acts like a stimulant in small doses, but it is an inhibitor in large doses.

5. Mech. Ageing Dev. 2005 126, 913-922

6. Mech. Ageing Dev. 2005 126, 987-1002.

7. Mech. Ageing Dev. 2006 127 8-15

Glucose versus lactate in immature brain slices

Brain metabolism,Energy Substrates,Ethics in science,Excitatory GABA,Lactate,Methodology,Neurodegenerative diseases,Neuroscience FAQ, Q&A — Tags: — 11:55 am

Related Q&A: “Y Ben-Ari writes that ‘Zilberter and Bregestovski and colleagues’ dealt with ‘ketone body metabolites’. What does ketone body metabolite mean? ”

About this post

1. These quotes were first used by Elly Strammer at F1000.com. After she agreed to remove her post from there, she contacted us suggesting that we use the quotes. We thank Elly for her contribution and for further commenting at the Naturally Selected

2. We received many questions regarding this post, quite a few of them concerned the formatting, which was not helping to clearly understand the issue. Because of that, we updated the post making sure to visually indicate quotes belonging to the arguing sides (according to F1000.com) . Now, remarks related to comments concerning the works of Y. Zilberter et al. are marked as  and remarks by Y. Ben-Ari are marked as 

 ”We demonstrate that in the neonatal brain, Em [membrane potential] and EGABA [reversal potential of GABA-induced anionic currents] strongly depend on composition of the energy substrate pool. Complementing glucose with ketone bodies, pyruvate or lactate resulted in a significant hyperpolarization of both Em and EGABA, and induced a radical shift in the mode of GABAergic synaptic transmission towards network inhibition.” (1)

“The main conclusions of our work are that the inhibitory effect of L-lactate on GDPs is not mediated by mitochondrial energy metabolism, and that glucose at its standard 10 mM concentration is an adequate energy substrate for neonatal neurons in vitro.” (2)

 ”We show that in the presence of glucose, lactate is effectively utilized as an energy substrate, causing an augmentation of oxidative metabolism. Moreover, in the absence of glucose lactate is fully capable of maintaining synaptic function. Therefore, during network activity in neonatal slices, lactate can be an efficient energy substrate capable of sustaining and enhancing aerobic energy metabolism.” (3)

“Lactate is not an efficient replacement for glucose and, as in vivo glucose is always kept at 4-5mM in the brain even in conditions of severe stress.” (4 a)

“The fact is, in the extracellular fluid (ECF) in the brain, glucose concentration is between 1.9 mM and 0.59 while lactate concentration is between 5.1 mM and 0.78 mM (for review, see [9 in this post]). The question arises: why 10 mM glucose in standard ACSF is adequate but 10 mM lactate is not.” (5)

“Clearly, the suggestions of Zilberter and colleagues rely on wrong assumptions and results that have not been reproduced.” (4 a)

“The effect of weak acids on GABA reversal potential and GDP generation was initially described for 4-5 mM concentrations of BHB [ketone body beta-hydroxybutyrate] (Rheims et al. 2009 ), lactate and pyruvate (Holmgren et al. 2010), and was later confirmed by independent research groups for similar concentrations of pyruvate (Tyzio et al. 2011), lactate and propionate (Ruusuvuori et al. 2010).” (6)

“From a clinical perspective, it is interesting to stress that relying on their observations on the positive actions of lactate on metabolism, Zilberter and colleagues have suggested that administration of lactate may be “a novel therapeutic tool to cure Parkinson, Alzheimer, Leigh syndrome and epilepsies” (4a)

 From Brain Fuels: This quotation is taken out of context. The exact piece from (9) reads: “… a growing body of evidence shows that metabolic stress caused by impaired energy homeostasis is a common feature of neurodegenerative disorders (NDDs) such as Alzheimer disease, Leigh syndrome, epilepsy, dementia, multiple sclerosis, neuropathies or ataxias [88] and [89]. We speculate that endogenous ES such as lactate, BHB and pyruvate or their combinations can be efficient in treatingNDD, and would address the cause rather than symptoms. Indeed, the neuroprotective effects of pyruvate have been repeatedly demonstrated in cases of brain ischemia, hypoglycemia, hemorragia, stroke and kainate-inducedepileptic brain damage[90], [91], [92]and [93]. Further research into mechanisms of the effects of ES on fundamental neuronal properties might allow more rapid progress in preventing and managing NDDs.”

The comment made on 29 Jul 2011 (4 b) quoted this paragraph with the references removed thus attributing the text solely to (9).

“Considering the compelling and well-known clinical observation that high lactate level is a classical sign of neuron suffering and severe conditions that require rapid intervention, this suggestion is, to say the least, astonishing.” (4 a)

“The bulk of the evidence suggests that lactate is an important intermediary in numerous metabolic processes, a particularly mobile fuel for aerobic metabolism, and perhaps a mediator of redox state among various compartments both within and between cells. Lactate can no longer be considered the usual suspect for metabolic ‘crimes’, but is instead a central player in cellular, regional and whole body metabolism… we might term the period from the 1930s to approximately the early 1970s the dead-end waste product era.” (7)

” It is curious that Dr Zilberter and colleagues refer to metabolism but have never reported measuring it.” (4 b)

“…Ivanov et al. (2011) simultaneously recorded oxygen tension, NAD(P)H fluorescence transients and local field potentials during electrical stimulation of the hippocampal Schaffer collateral pathway in neonatal brain tissue slices from mice. From the very beginning, the authors took great care to ensure both viability and functionality of their preparations. They convincingly demonstrated that surprisingly high superfusion rates with standard artificial cerebrospinal fluid (ACSF) in the slice chamber are required to ensure adequate oxygenation and complete electrical function in blood-free tissue slices. An important implication of this methodological tour de force is that under many previously reported experiments the requirements for viability may been met while the functionality may have been compromised.” (8)

References

  1. Holmgren, C. D., Mukhtarov, M., Malkov, A. E., Popova, I. Y., Bregestovski, P., and Zilberter, Y. (2010). Energy substrate availability as a determinant of neuronal resting potential, GABA signaling and spontaneous network activity in the neonatal cortex in vitro. J. Neurochem. 112, 900–912.
  2. Ruusuvuori E et al. (2010). Spontaneous network events driven by depolarizing GABA action in neonatal hippocampal slices are not attributable to deficient mitochondrial energy metabolism. J Neurosci. Nov 17; 30(46):15638-42
  3. Ivanov A, Mukhtarov M, Bregestovski P and Zilberter Y (2011) Lactate effectively covers energy demands during neuronal network activity in neonatal hippocampal slices. Front. Neuroenerg. 3:2.
  4. Ben-Ari Y.  a) Faculty of 1000, 06 Jan 2011, evaluation,  b) 29 Jul 2011, comment.
  5. Zilberter Y. Faculty of 1000, 19 May 2011 and July 14 2011, comments.
  6. Khakhalin A (May 18, 2011). Questioning the depolarizing effects of GABA during early brain development. J Neurophysiol doi: 0.1152/jn.00293.2011.
  7. Mendel I. Faculty of 1000, 04 Jun 2011, comment (Currently the comment is removed).
  8. Kasischke K (2011) Lactate fuels the neonatal brain. Front. Neuroenerg. 3:4. doi: 10.3389/fnene.2011.00004
  9. Zilberter Y, Zilberter T, Bregestovski P. (2010) Neuronal activity in vitro and the in vivo reality: the role of energy homeostasis. Trends PharmacolSci 31:394–401.

LTP induction and AMPA

Neuroscience FAQ, Q&A — Tags: , — 8:10 am

 

Q&A and FAQ (archived) :: Ongoing Q&A :: Neuroscience Q&A and FAQ

QUESTION 1: When you say ‘LTP induction’, does it mean increasing number of AMPA receptors?
Sujin
ANSWER 1:Hi Sujin,Long-term potentiation (LTP) is considered a neuronal analog of memory so I do not think that “increasing number of AMPA receptors” fully describes the process. The trafficking of AMPA receptors to synapses is thought to be one of mechanisms. During LTP induction, there is an increased delivery of AMPA receptors to synaptically active regions without changes in receptor affinity (1), by exocytosis to stimulated spines (2). This delivery precedes the full expression of LTP (3).

I suggest that you read the latest review article “AMPA receptor regulation during synaptic plasticity in hippocampus and neocortex” in Seminars in Cell & Developmental Biology doi:10.1016/j.semcdb.2011.06.007.

Sources

1. J Physiol, 2004, 559, 543-554

2. PNAS, 2010 vol. 107, 36, 15951-15956

3. PNAS, 2008 vol. 105, 32, 11388-11393

QUESTION 2 : First of all, thank you very much.

But I am curious about this… you mean AMPA receptors were already made, stored in somewhere and when it is needed, go to synaptically active regions?

If I am right, where were they stored in?

p.s I can’t speak English very well. I hope you understand.

ANSWER 2: I perfectly understand you, don’t worry.

Most of AMPA receptors are located within neuronal cytoplasm. As to their expression, there’s, for example, a special protein (NSF) involved in neurotransmitter release from the presynaptic terminal that binds to the GluR2 subunit of AMPA and regulates surface expression of AMPA receptors. It can get too complicated to give you more details and I am not sure about the level of your basic knowledge so please don’t hesitate telling me more about your interest.

 

Tanya Zilberter


Dream control, conscious dreaming

Neuroscience FAQ, Q&A — Tags: , , , — 2:27 pm

Q&A and FAQ (archived) :: Ongoing Q&A :: Neuroscience Q&A and FAQ

Question

First of all, thank you for your time. I realize that this is on a volunteer basis and that you do this for nothing but smiles. Thank you.

Now,I have recently begun getting interested in Lucid Dreaming, after having experienced it a few times, and am now trying to practice it to where I can do it every night. Since sleeping is when your brain organizes information, can shaping my dreams to my will stop that process?

Also, I’ve read that there are “practical” applications of Lucid Dreaming, but all of them seem to be about nightmare therapy or some other type of therapy.

My question here being: Could you use Lucid Dreaming to practice something in a “real life” application that you learned early in the day?

Answer

Dear Ryan,

First of all, you might want to read my answer to a similar question, although connected to a difference situation, in the blog post Lucid dream – sleep or wakefulness? As to the practical application, there indeed are quite a few techniques and interesting researches. For instance, lucid and control dreams were associated with all electronic media use but most strongly with video game play (Electronic media and lucid-control dreams: Morning after reports. By Gackenbach, J. Dreaming, Vol 19(1), Mar 2009, 1-6). You might read a full text, not too technical commentary on “The neurobiology of consciousness: Lucid dreaming wakes up” by J. Allan Hobson. However, the scholarly conclusion is so far that there’s a “poor reliability of lucid dream induction techniques (for a review, see Price & Cohen (1988). Lucid dream induction. An empirical evaluation. In: Conscious mind, sleeping brain.Perspectives on lucid dreaming (pp. 105-134). NY: Plenum Press).

If however you don’t need scientifically proved methods, there’s anecdotal evidence of control upon dream content, for instance, in the Silva Method, which is essentially guided imagery.

To your question whether it can stop the processing of information in the brain, I am not aware of reliable research results confirming this idea. I’ll double-check it and if I’m wrong, I’ll update my answer.

Tanya Zilberter

What can be done to fight off Alzheimer’s disease?

Alzheimer's,Neuroscience FAQ, Q&A,Parkinson's,Pyruvate — 12:41 pm

Q&A and FAQ (archived) :: Ongoing Q&A :: Neuroscience Q&A and FAQ

Question
I’ve read on WebMD that there’s no evidence that anything can be done to fight off Alzheimer’s disease. But I also read the opposite opinions. What is yours? – Donna

Answer
Dear Donna,

You probably mean the following conclusion cited by WebMD:

“There is currently no evidence considered to be of even moderate scientific quality supporting the association of any modifiable factor (nutritional supplements, herbal preparations, dietary factors, prescription or nonprescription drugs, social or economic factors, medical conditions, toxins, environmental exposures) with reduced risk of Alzheimer’s disease,” concludes the report, issued by a National Institutes of Health consensus panel on Alzheimer’s prevention.”

I am surprised that they haven’t mentioned exercise, for which, in my humble opinion, a solid body of evidence exists and the caffein research, for which intricate mechanisms are being researched. Also, quite a few harmful influences such as hydrogen peroxide, glutamate, zinc, and copper/cysteine were convincingly reported. I added caffein effects on another neurodegenerative disease, the Parkinson’s but I know of similar studies in Alzheimer’s.

Walking away from dementia

Coffee, tea, and chocolate can help to avoid Parkinson’s disease

Pyruvate protects neurons against A-beta peptides characteristic for Alzheimer’s
Tanya Zilberter

Do we subconsciously know the time?

Neuroscience FAQ, Q&A — Tags: , , , — 11:17 am

Q&A and FAQ (archived) :: Ongoing Q&A :: Neuroscience Q&A and FAQ

Question

Do we subconsciously know the time? Some people reported experiences which may show evidence to that.
Also, I heard that some people with mental disorders such as autism can tell time without a clock.

This may be due to brain mutations causing some of the subconscious to be “elevated”, if you will, into the *conscious* mind.

Also, some people can wake up without an alarm clock, which also supports this theory in my view.

Is any of my information correct? Do you agree with any of my ideas?

Please explain this in more depth. Thanks.

Answer

Hello,

You asked at least two questions and I’ll answer what I know about time perception in autistic people (not so easy to find on the Net) and suggest you some reading for the working with subconscious.

1. Time perception

There’s anecdotal evidence of the increased attention drive in people with autism. It can explain some of the (also anecdotal) evidence regarding their unusual memory, computation, decision making or image recognition abilities. However, not all autistics are created equal; because of that, researchers talk about Autistic Spectrum Disorders. Some people with ADS have IQs high enough and are communicative enough to perform in psychometric tests, but some are not and we know little about this group’s abilities.

As to the time perception, researchers talk about different parameters. For example, Drs Wallace and Happe at Institute of Psychiatry, Kings College London, London, UK (Research in Autism Spectrum Disorders 2, 2008, 447–455), studied three of them (quote):

a) Time estimation: Using a stopwatch, the experimenter says ‘‘Go’’ and ‘‘Stop’’ after the passage of a pre-designated time period (e.g., 45 s) and subsequently asks the participant to estimate how much time has passed.

b) Time production: The participant is asked to say ‘‘Go’’ and ‘‘Stop’’ when s/he thinks a designated amount of time (e.g., 12 s) has passed.

c) Time reproduction: The experimenter says ‘‘Go’’ and ‘‘Stop’’ after a pre-designated time passage, and then requests the participant to copy this time passage by saying ‘‘Go’’ and ‘‘Stop’’. (unquote).

Perception of shorter periods of time has been investigated previously (Br J Psychology, 95, 2004 269–282). This study showed that people with ASD are somewhat deficient in reproducing intervals of  of 2–3 seconds.

2. Subconscious <-> conscious

It’s a huge theme! There are tons of stunning information about phenomena concerning the two-way exchange, some of which is considered normal, some not. The basis for difficulties of this exchange in normal conditions is similar (I think) to the process of forgetting. Is forgetting bad? In many cases, yes, but normally, it is absolutely necessary for brain’s functioning.

The cases of inability to forget are descried (for example, the brilliant book by Alexander Luria “The Mind of a Mnemonist: A Little Book about a Vast Memory”). The mind of such people seems to be quite different and their lives are not easy. Looks like people are better off when they respect the normal barrier between these two ways of our mind’s operation. Remember “Be Careful What You Pray for … You just Might Get It”?

However, some of practical psychotechniques can be helpful. I tried the Silva method (The Silva Mind Control Method ) and found it rational. I am aware of the subliminal methods, BTW, extremely successful in the advertising industry.

Read more:
 Working with the subconscious (search results)
 The Silva method
 The Mind of a Mnemonist

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