Medical Researcher-Mr

28/10/2023

Good News!

We will be working on Fish Vaccine and its impact to human health.

Any form of information and cooperations is highly welcome.

05/04/2020

What did you know about covid-19, and what did you wish to know. Share with us hear here let's be of help with each others. Heart you all

12/01/2020

Memories of traumatic experiences can lead to mental health issues such as post-traumatic stress disorder (PTSD), which can destroy a person’s life. It is currently estimated that almost a third of all people will suffer from fear- or stress-related disorders at one point in their lives.

Now, a new study shows – at the cellular level – how therapy can treat even long-term memories of trauma. “Our findings shed, for the first time, light onto the processes that underlie the successful treatment of traumatic memories,” says EPFL Professor Johannes Gräff of EPFL’s School of Life Sciences, whose lab carried out the study.

In the field of treating traumatic memories there has been a long-debated question of whether fear attenuation involves the suppression of the original memory trace of fear by a new memory trace of safety or the rewriting of the original fear trace towards safety. Part of the debate has to do with the fact that we still don’t understand exactly how neurons store memories in general. Although they don’t exclude suppression, the findings from this study show for the first time the importance of rewriting in treating traumatic memories.

Research in this area focuses on understanding the brain’s capacity to reduce traumatic memories, but surprisingly few studies have investigated treatment options for attenuating long-lasting trauma (aka “remote fear”) in animal models.

The EPFL scientists found that remote fear attenuation in the brain is connected to the activity of the same group of neurons that are also involved in storing these memories. Working with mice, the scientists have located these neurons in the brain’s dentate gyrus, an area of the hippocampus that is involved in the encoding, recall, and the reduction of fear.

The mice used in the study are genetically modified to carry a “reporter” gene that produces an identifiable and measurable signal, e.g. a fluorescent protein, following neuronal activity. Using a fear-training exercise that produces long-lasting traumatic memories, the scientists first identified the subpopulation of neurons in the dentate gyrus that are involved in storing long-term traumatic memories.

the dentate gyrus in the brain
Cross section of brain showing the dentate gyrus (“Gyrus dentatus” at bottom center). NeuroscienceNews.com image is credited to Henry Gray, Anatomy of the Human Body (1918).

The mice then underwent fear-reducing training, which resembles exposure-based therapy in humans – the most efficient form of trauma therapy in humans today. Surprisingly, when the researchers looked again into the brain of the mice, some of the neurons active at recalling the traumatic memories were still active when the animals no longer showed fear. Importantly, the less the mice were scared, the more cells became reactivated. This was a first hint that the same population of neurons may be involved in storing and attenuating traumatic memories.

The researchers then reduced the excitability of the recall neurons during the exposure therapy and found that the mice showed poorer fear reduction compared to controls. But when they reduced the excitability of other neurons in the dentate gyrus, there was no such effect, showing that the recall neurons in the dentate gyrus are crucial for fear attenuation.

Finally, when the researchers enhanced the excitability of these recall neurons during the therapeutic intervention, they found that the mice showed improved fear reduction. Thus, they concluded that attenuating remote fear memories depends on the continued activity of the neurons they identified in the dentate gyrus.

12/04/2019

31/05/2018

Hormone Therapy May Lead to Improved Cognitive Function

MAY 31, 2018



FEAT U RED NE URO LO GY NE URO S CIEN CE

3 M IN RE AD

1 Agar Agar Powder supplier 10+ Years Experience professional Agar Agar Manufacturer,quality guarantee,fast delivery foodchem.cn

2 Affordable Education Earn an up to 75%Scholarship from UNICAF apply.unicaf.org

3 Diabetes Solution Discover how to reverse diabetes with no side effect optimalhealthfocus.com

4 Is God Really Here? Yes - In Tragedy, God is Still There God Wants to Help You. See What You Can Count on God For. everystudent.com

Summary: A new study reveals using estradiol gel in combination with oral progesterone can help to improve cognitive function in postmenopausal women.

Hormones affect just about everything that goes on in a woman’s body, from reproductive function and sexual libido to weight gain and overall mood. A new study shows how, in the right dosage and combination, hormones also may slow cognitive decline in postmenopausal women as they age. The study is being published online today in Menopause.

It comes as no surprise that cognitive function declines as we age. We recognize memory decline in a number of ways, such as not being able to remember a grocery list as easily as we once did. Mild cognitive impairment (MCI) is defined as that intermediate stage between normal aging and dementia. Persons with MCI have an increased risk of progressing to Alzheimer disease or other dementia, with roughly 20% of this population crossing over from MCI to a more severe level each year. To date, no pharmacologic treatment has proven effective in managing MCI.

The study followed postmenopausal women who were diagnosed with MCI and taking donepezil over a 24-month period and showed that cognitive test scores for the women who received hormone therapy significantly increased during that time.

The article “Menopausal hormone therapy

Posted on April 16, 2018Hello world! Welcome to WordPress. This is your first post. Edit or delete it, then start writing!

27/04/2018

In the largest study of its kind, a three-minute
version of a brain stimulation treatment was
shown to be just as effective as the standard
37-minute version for hard-to-treat depression.
These results were published in a new Canadian
study in The Lancet co-led by the Centre for
Addiction and Mental Health (CAMH) and the
University Health Network’s Krembil Research
Institute, in collaboration with the University of
British Columbia.
The treatment is called repetitive transcranial
magnetic stimulation (rTMS), which is a form of
treatment that uses magnetic field pulses to non-
invasively stimulate a part of the brain called the
dorsolateral prefrontal cortex, which is
associated with mood regulation. The study
compared standard rTMS treatment, which uses
high frequency (10 Hz) brain stimulation for 37.5
minutes per session, with a newer form of rTMS
called intermittent theta burst stimulation (iTBS)
, that mimics the brain’s natural rhythms and
takes just over three minutes per treatment.
“The main impact of this study is that the
number of people who are able to be treated
using theta burst stimulation compared to the
standard form of rTMS can be increased by three
to four fold,” says lead author Dr. Daniel
Blumberger, Co-Director of the Temerty Centre
for Therapeutic Brain Intervention at CAMH.
“These findings will have a significant impact on
our ability to treat patients,” says Dr. Jonathan
Downar, Co-Director, University Health
Network’s rTMS Clinic; Scientist, Krembil
Research Institute and senior author of the
study. “This will allow every device in Canada to
treat several times more people per day, meaning
shorter wait lists and better access to this
treatment.”
The study, conducted with Dr. Fidel Vila-
Rodriguez, Assistant Professor, University of
British Columbia, focused on people with
treatment-resistant depression, defined as a
condition whereby people do not experience a
sufficient improvement in their symptoms after
trying antidepressant medications. Up to 40 per
cent of people with depression may experience
treatment resistance.
In the study, 414 participants were randomly
allocated to receive either the standard form of
rTMS treatment or the shorter iTBS treatment
for five days a week for up to six weeks.
In the study, 414 participants were randomly
allocated to receive either the standard form of
rTMS treatment or the shorter iTBS treatment
for five days a week for up to six weeks.
NeuroscienceNews.com image is in the public
domain.
For 49 per cent of study participants who had the
iTBS treatment, depression symptoms reduced
significantly, with 32 per cent reporting a
remission of depression symptoms. Those who
received standard rTMS had a remission rate of
27 per cent. Those results are consistent with
previous large-scale studies and meta-analyses
over the past 20 years that have confirmed the
efficacy and safety of the standard form of
rTMS.
rTMS treatment was approved for treating
depression by Health Canada in 2002 and by the
U.S. Food and Drug Administration in 2008. Due to
the cost of treatment (it is not covered by public
health insurance outside Quebec and
Saskatchewan), it has only been made available
to a fraction of the estimated 600,000 Canadians
living with treatment-resistant depression each
year.
“rTMS has changed my life in so many ways,”
says study participant Shelley Hofer, 43, who has
had treatment-resistant depression for most of
her life. “I really wish it had been around a long
time ago because I believe it would have been my
go-to treatment. In my personal opinion, I feel
rTMS could improve the lives of so many people
who are still struggling to find the answers to
their own mental illness.”

Neuroscience News provides research news for neuroscience, neurology, psychology, brain science and cognitive sciences.

04/01/2018

WE WISH ALL OUR FANS HAPPY SURVIVAL OF THE YEAR 2017 AND ALSO HAPPY NEW YEAR. MANY MORE OF WITH GOOD HEALTH,PEACE AND WEALTH. PROMISE TO SERVE YOU BETTER IN THIS YEAR. ONCE AGAIN HAPPY NEW YEAR

07/12/2017

Healthy Mitochondria Could Stop Alzheimer’s

Summary: Boosting mitochondria may defend against a form of protein stress that can reduce the formation of amyloid plaques.

Alzheimer’s disease is the most common form of dementia and neurodegeneration worldwide. A major hallmark of the disease is the accumulation of toxic plaques in the brain, formed by the abnormal aggregation of a protein called beta-amyloid inside neurons.

Still without cure, Alzheimer’s poses a significant burden on public health systems. Most treatments focus on reducing the formation of amyloid plaques, but these approaches have been inconclusive. As a result, scientists are now searching for alternative treatment strategies, one of which is to consider Alzheimer’s as a metabolic disease.

Taking this line of thought, Johan Auwerx’s lab at EPFL looked at mitochondria, which are the energy-producing powerhouses of cells, and thus central in metabolism. Using worms and mice as models, they discovered that boosting mitochondria defends against a particular form of protein stress, enables them to not only protect themselves, but to also reduce the formation of amyloid plaques.

Whole-brain hemisphere sections of Alzheimer’s mice, the model APP/PSEN1, before and after treatment with the NAD+ booster Nicotinamide riboside (NR). The beta-amyloid plaque content in the brain of the APP/PSEN1 mice (left), clearly visible by Thioflavin S staining in green color and associated to brain damage during the disease, is reduced after 10 weeks treatment with NR (right).

During normal aging and age-associated diseases such as Alzheimer’s, cells face increasing damage and struggle to protect and replace dysfunctional mitochondria. Since mitochondria provide energy to brain cells, leaving the

Neuroscience News provides research news for neuroscience, neurology, psychology, brain science and cognitive sciences.

12/11/2017

Studying Sleep’s Profound and Extensive Effects on Brain Function

Summary: Studies presented at Neuroscience 2017 shed new light on how the brain consolidates memories and the neurological effects of poor sleep.
Source: SfN.
Although the general benefits of a good night’s sleep are well established, one-third of American adults do not get a sufficient amount of sleep. Recent research sheds new light on the extensive effects of sleep on the brain, as well as the harms caused by sleep loss. The studies were presented at Neuro2017, the annual meeting of the Society for Neuroscience and the world’s largest source of emerging news about brain science and health.
Adequate restful sleep leads to improved cognitive function and enhanced memory formation, while insufficient, restless sleep has harmful effects such as impaired memory and judgement, and can lead to increased risk for medical conditions such as stroke, obesity, and cardiovascular disease. The connection between sleep and brain function has long been an area of exploration for neuroscientists.
Today’s new findings show that:
MicroRNA expression may serve as an indicator of sleep loss in rats and humans, suggesting a possible method for predicting those at risk for diseases and cognitive deficits typically associated with sleep debt.
Three species of spiders have amazingly fast circadian clocks, raising questions about how they avoid the negative effects typically associated with deviating from the normal biological timeframe.
The brain preferentially reactivates negative memories during sleep, prioritizing the retention of these emotional memories.
Other recent findings discussed show that:
A computerized algorithm can determine whether people viewed images of faces or houses by comparing patterns of electrical activity in the brain during sleep.
“Sleep is even more multifaceted and fascinating than we realize,” said press conference moderator Sigrid Veasey, a professor at the Center for Sleep and Circadian Neurobiology at the University of Pennsylvania’s Perelman School of Medicine. “Today’s findings reveal interesting new aspects of the complex relationship between sleep and the brain, and the vital role that sleep plays in everyday human functioning.”

02/11/2017

For a decade, the Yale team had sought answers to a fundamental question: How does the brain, marked by frantic growth of synaptic connections between cells, grow up and mature?
“Up until early adulthood, synapses between cells are wild, more plastic; they shrink and grow and even destabilize sister synapses,” said senior author Anthony Koleske, professor of molecular biophysics and biochemistry and of neuroscience. “In mature brains, synapses become much more restrained, they are smaller and more well-behaved.”
The new research identifies the crucial signal in the taming of the adolescent mind as fragments of a family of proteins called laminins, which are crucial to neuromuscular functioning among other biological functions.
The researchers found that mice lacking the laminin alpha 5 gene suffered defects in synapse maturation, leading to fewer synapses by early adulthood.
Laminins had been overlooked by synapse researchers because their relatively large size made them unlikely to function within the tight space of synapses in the in the brain. The new findings suggest that fragments of the protein bind to receptors of the synapse in adolescent brain, triggering the maturation process, Koleske said.
“Our synapses change when we learn new things, but in order to retain what is learned, synapses must stabilize,” said Mitchell H. Omar, a graduate student in Koleske’s lab and lead author of the study.
Partial failure of this key signaling pathway may play a role in onset of neuropsychiatric disorders such as schizophrenia, which typically appear during late adolescence, Koleske said.

07/10/2017

we are there for your good health