Good sleep promotes communication between your neurons (by inducing formation of new synapses).

A good night sleep is essential for refreshing oneself after a hectic day. It’s now known to us that sleep is essential not only for healthy body, but also for healthy mind. The role of sleep in the consolidation of memory has already been established. But the cellular and molecular processes behind this sleep induced memory consolidation are not yet known.

Researches have shown conflicting views regarding the role of sleep in synaptic plasticity. Some research supports the idea of synaptic down-scaling, whereas other supports the idea of synaptic up scaling during sleep.

A study conducted by Yang et al at New York University, School of Medicine, showed that sleep promotes formation of post-synaptic dendritic spines on a subset of branches of individual layer V pyramidal neurons in the mortor cortex of mice.

The study can be divided into two parts. In 1st part, they assessed spine formation following training. For this, they used two groups of mice. The experimental group consisting of mice that were given motor training for 2 days and the control group consisting of untrained mice. Rotarod motor training was given to the experimental group. The results were analyzed based on  time frame of experiment. Firstly, within 6 hours of motor training and then within 24 hours and after 24 hours of motor training. In 2nd part, they gave rotarod training to mice and divided the mice into two categories: non-sleep deprived and sleep deprived mice.  Then, they assessed the formation of new dendritic spines in sleep deprived vs non sleep deprived mice.

The results showed significantly higher formation of dendritic spines in trained mice in first 6 hours of training as compared to untrained controls. This formation of dendritic spines in trained mice was continuous in the 1st day. The spine formation remained confined to about 30% of dendrities after 24 hours of motor learning.  Likewise, there was significant reduction in dendritic spines in  sleep deprived mice as compared to non-sleep deprived mice. The reduction in the dendritic spines after sleep deprivation cannot be compensated either by motor training or by sleeping again.

Sleep consist of two phases: Rapid eye movement(REM) phase and NREM(non rapid eye movement) phase. Sleep deprivation in  REM phase did not disrupt the  formation of dendritic spines. Its in the NREM phase of sleep that dendritic spines are formed. Also, the study showed via calcium imaging that it’s the same neurons that are activated during neuronal activation at wakefulness and NREM phase of sleep. This neuronal reactivation during NREM phase is critical in the formation of new dendritic spines.

Concluding the results, rotarod training is important for the formation of new synapses as shown by increase in dendritic spines in trained mice as compared to untrained controls in the 1st part of the experiment. However, there was significant reduction of dendritic spines in sleep deprived mice undergoing motor training  suggesting that sleep is necessary for  formation of new synapses after learning. Formation of new synapses after learning occurs during NREM phase of sleep and neuronal reactivation is responsible for it.

Reference:

Guang Yang et al, Sleep promotes branch-specific formation of dendritic spines after learning, Science 344,1173 (2014); DOI: 10.1126/science.1249098

Fearing dementia during old age??Vitamin B might be the solution!!!!

Vitamin B12

Sources of Vitamin B12

Vitamin B12 is a water soluble vitamin which has a wide range of function including DNA synthesis and myelination of neurons. A new research study published by University of Oslo has shown yet another vital role of Vitamin B12 in neurological diseases. People suffering from early stage cognitive impairment called Mild Cognitive impairment(MCI) and impending dementia will benefit from the new discovery.The findings of the research have shown Vitamin B12 to be effective in preventing Alzheimer’s disease, especially in those who have high level of homocysteine in their body. Homocysteine is an amino acid, which is thought to be involved in the formation of neurofibrillary tangles in the neurons, thus disrupting the communication between neurons and giving rise to AD. There is a direct proportional relation between increased blood homocysteine level and the rise in mild cognitive impairment.

An elevated level of homocysteine can be reduced by administering Vitamin B12. It can be administered orally, or via injection. But the dose of Vitamin B12 in these persons must be higher than the normal dietary requirement.

What are the sources of Vitamin B12?

Sources of Vitamin B12: Sea foods like salmon, shrimps, sardines; milk and milk products; eggs,red meat and liver and legumes. Vegetarians must be careful to avoid dietary deficiency of Vitamin B12. It’s advisable for the vegetarians to take Vitamin B12 capsules. Similarly, elderly people and those who consume excessive alcohol might have poor absorption of this vitamin. In these cases, it’s better to check your Vitamin B12 level regularly and take the parenteral (injection) form of Vitamin B12.

Reference:

http://www.med.uio.no/imb/english/research/news-and-events/news/2013/vitamin-b-impedes-development-of-alzheimer%E2%80%99s-.html

Withania Somnifera (Ashwagandha) and its neuroprotective effects

What is Ashwagandha or Withania Somnifera?

Withania Somnifera(WS), also called Ashwagandha in Sanskrit is a herbal plant widely mentioned and used in ayurvedic medicine. In Ayurveda, Ashwagandha is used to enhance mental health and memory and research have proved that it, in fact, enhances memory. Recent studies have also shown that the ashwagandha root have other wide range of therapeutic properties like antistress, immunomodulatory and antioxidant.

Berry of the Withania somnifera plant

Berry of the Withania somnifera plant

Ashwagandha its use in neurodegenerative diseases:

The roots of Ashwagandha extracts have shown to reduce the number of hippocampal degenerating cells significantly in the brains of stressed rodents and were neuroprotective in animal models of Parkinson’s disease.

Studies done in rats at Defense Institute of Physiology and Allied Sciences, India have shown that withania somnifera roots can improve the hypobaric hypoxic induced memory impairment and neuronal degeneration. Likewise, study done in Human neuronal cells at Herbert Wertheim College of Medicine, USA showed that Ashwagandha(Withania Somnifera) benefits in Alzheimer’s disease(AD). It shows neuroprotective effects in AD.

Animal studies have shown that withania somnifera reverses the behavioral deficits, plaque pathology and accumulation of β-amyloid peptides (Aβ) in the brain. The roots of WS reverse the effect of beta amyloid induced toxicity in AD. Accumulation of β-amyloid is known to be one of the major pathogenesis associated with AD. Thus withania somnifera (WS) extracts can be used as an agent for the prevention of AD. β-amyloid and ashwagandha treated cells  showed no reduction in spine density, spine area, spine length and number of spines as compared to untreated control thus showing the protective effect of ashwagandha on spine density. It is the reduction of spine area, spine length and number of spines which are related to neurodegenerative diseases causing decrease in synaptic plasticity and thus compromising learning and memory. Study done at Chonbuk National University, South Korea has shown that WS stimulates the NMDA receptor in hippocampal cells which is the brain area important for learning and memory.

So, Ashwagandha is an important herb and recent studies have shown promising results regarding its medical benefits, nevertheless in neurodegenerative diseases.

References:

Janardhan Prasad Bhattarai, Soo Joung Park, and Seong Kyu Han, Potentiation of NMDA receptors by Withania somnifera on hippocampal CA1 pyramidal neurons

Am. J. Chin. Med. 41, 503 (2013). DOI: 10.1142/S0192415X13500365

Baitharu I, Jain V, Deep SN, Hota KB, Hota SK, Prasad D, IIavazhagan G, Withania somnifera root extract ameliorates hypobaric hypoxia induced memory impairment in rats.

J Ethnopharmacol. 2013 Jan 30;145(2):431-41. doi: 10.1016/j.jep.2012.10.063. Epub 2012 Dec 2

Kurapati KR, Atluri VS, Samikkannu T, Nair MP, Ashwangha (Withania somnifera) Reverses β-amyloid 1-42 Induced Toxicity in Human Neuronal Cells: Implications in HIV-Associated Neurocognitive Disorders (HAND) PLoS One. 2013 Oct 16;8(10):e77624. doi: 10.1371/journal.pone.0077624

Sleep important for myelin formation in brain

What is Myelin?

Myelin is a fatty sheath that insulates the neurons. It is needed for the fast propagation of signals(saltatory conduction) through neurons. Oligodendrocytes and Schwann cells are responsible for its production in central nervous system and peripheral nervous system respectively. Myelin producing cells in brain are different from neuronal cells as they lack the electrical properties of neurons. They are also called interstitial cells of brain.

The newly discovered relationship between sleep and myelin forming cells:

A recent research published in journal of neuroscience have shown that sleep is vital in the proliferation of oligodendrocytes precursor cells(OPC). Its the OPCs that differentiate into oligodendrocytes during sleep. This means sleep induces the formation of oligodendrocytes in neurons. This research does not tell anything about schwann cells which are responsible for myelin formaion in peripheral neuron.

Why is this finding important?

This finding might be important for neurodegenerative diseases like multiple sclerosis where there is loss of myelin.

This further highlights the molecular impact of sleep on brain cells. Not only the sleep beneficial for neuronal cells, but also for interstitial cells like oligodendrocytes.

More oligodendrocytes after sleep means more myelin in your neurons and thus more effective signal propagation.

References and for further reading:

http://www.bbc.co.uk/news/health-23932577

http://www.dailymail.co.uk/health/article-2411833/Sleep-helps-boost-brain-cell-production-Findings-insight-role-rest-brain-repair-growth.html

Sleep for better memory

Figure: fromWikipedia

A good sleep is needed for good life. And this is true for the brain as well. Sleep has a lot of things to do with brain especially memory.

Sleep has two phases: NREM (Non rapid eye movement) phase and REM (Rapid eye movement or deep sleep). Its during REP phase short term memory(memory lasting second to hours) is consolidated and converted into long term memory( Last for a very long time with unlimited capacity). For the formation of long term memory, there should be change in the structure of neurons as well as dissipation of information from hippocampus to other parts of brain mainly cerebral cortex.

It has been proved scientifically that sleep is important for memory as it’s the period during which our memory is consolidated.Generally, an average of 8 hours of sleep is good for the brain. Taking nap in between your studies helps in memorizing the contents. For example, taking nap every half an hour or 15 minutes after a study period of 2 or 3 hours helps you memorize better than studying continuously for an entire day.

So, managing your sleep along with your study might make you smart.