Tuesday, 7 August 2018

Neuroscience 2019 Conference at Berlin, Germany

PULSUS brings in a new spin on conferences by presenting the latest scientific improvements in your field. Listen to motivating keynotes from thought leaders, or rub elbows with pioneers across the globe. Berlin is all set for an amazing event as PULSUS proudly presents the “2nd Annual Congress on Advancements in Neurology and Neuroscience” slated on March 11-12, 2019 at Berlin, Germany. The theme of the conference is “Exploring the Modern Trends and Innovations in Neurology and Neuroscience”.

Submit your abstracts and be a part of the #experts gathering.
For more details:

Friday, 1 June 2018

Neuroscience  Facts

Ø  Social Ties Preserve Memory, Slow Brain Aging
A strong social network could be the key to preserving memory. New research has found that mice housed in groups had better memories and healthier brains than animals that lived in pairs.

Ø  For Anxiety, a Single Intervention Is Not Enough
No matter which treatment they get, only 20 percent of young people diagnosed with anxiety will stay well, researchers report.

Ø  Memory Depends On Protein 'Off-Switch'
Memory, learning and cognitive flexibility depend on a protein 'off-switch' in the brain, according to a breakthrough discovery.

Ø  Hormone Therapy: Better Cognitive Function?
A new study shows how, in the right dosage and combination, hormones also may slow cognitive decline in postmenopausal women as they age.

Wednesday, 30 May 2018

Workshop  on Different optic Neuropathies and Novel Treatments

Umur Kayabasi, 

Bahcesehir University, Turkey


The aim of this workshop is to discuss the diagnosis, treatment and follow- up of different optic neuropathies. Meanwhile images from the new technology devices like OCT and the conventional machines like Perimetry will be shown. Also MR images of the orbit and brain and images of optic nerve problems will be the subjects of the main topic. There are some new developments in the treatment of the optic neuropathies and different ideas about novel treatments will be shared.

OPTİC NEUROPATHİES:  Optic neuritis ( demyelination of the optic nerve): Acute, painful vision loss. Occurs mainly in women within the age range of 18- 45. Responds well to high dose intravenous steroids. Approximately 1/3 of the cases are seen with disc edema, 2/3 are retrobulber. Retrobulber cases progress to multiple sclerosis (MS ) more frequently. The possibility of a woman patient to develop MS after isolated optic neuritis is about % 70 in ten years. The progression of optic neuritis to MS can be detected by OCT.

Anterior ischemic optic neuropathy (non- arteritic): Acute, painless visual loss due to a stroke on the optic nerve head. Disc edema is present. Patients usually have hypertension or diabetes. Visual field defect is altitudinal. Cup to disc ratio is small. No definite treatment. Intravitreal injections (triamcinolone and anti- VEGF) may be tried in acute cases. 

Traumatic optic neuropathy: Occurs after a direct or indirect trauma to the optic nerve. Steroids are not recommended if there is head concussion. Surgery of the optic canal to decompress the nerve may be tried in early stages. There are reports about success with intravenous erythropoietin.
Toxic optic neuropathy: Central, bilateral visual loss. There is a new report about improvement after methanol toxicity with the combination of erythropoietin and steroids.

Radiation optic neuropathy: Bilateral visual loss months or years after radiation therapy of a brain tumor. There are new reports of improvement of vision with intravenous bevacizumab tharapy.

Leber’ s optic neuropathy: Painless,bilateral visual loss with central scotomas. Inherited by the maternal mitochondrial DNA mutations: m.11778, m.14484, m.3460. Idebenone treatment in early stage Leber?s disease have been shown to be beneficial. 

Chronic relapsing inflammatory optic neuropathy: Steroid sensitive optic neuropathy which recurs after steroid withdrawal. Long term steroids or other immunosuppressive agents are used. There are other optic neuropathies with inflammatory, infectious, etc. etiology which can be discussed, too.

Monday, 28 May 2018

Special Opportunities for #Graduates, Post Graduates and #Research scholars under Young #Scientist Category. Neuroscience2018 invites participants from all over the world.

Thursday, 24 May 2018

Neuroscience 2018 proudly announces #Bence Andras as an invited Speaker for the conference Annual Congress on Advancements in Neurology and Neuroscience scheduled on June 18-19, 2018 at #Rome, #Italy.

Wednesday, 23 May 2018

What Causes Prion Disease?

Prion diseases are associated with the build up in the brain (and some other organs) of an abnormal or ‘rogue’ form of a naturally occurring cellular protein, known as the prion protein. The rogue protein results from a change in shape of the normal prion protein.  Once formed in the body these rogue proteins recruit and convert more of the normal prion protein into the abnormal form, setting off a kind of chain reaction which leads to a progressive accumulation of the rogue protein.  In the normal course of events, once they have served their purpose, prion proteins are broken down by enzymes in the body.  The abnormal prions however are more resistant to this process; so they accumulate and cause damage in the brain, which interferes with normal brain functioning.  All forms of the disease are thought to be associated with an incubation period.  This is a clinically 'silent phase' during which replication of the rogue protein is thought to be taking place.


Genetic Susceptibility

At a particular position in the prion gene known as codon 129, there are two possible genetic types, which in turn specify the body to produce different amino acids at this position.  These amino acids are called methionine and valine, or M and V for short.  In most countries, MM and MV frequencies in the population are roughly equal (40-50%).  It has been known for some years that individuals, who are MV, are at much less risk of developing prion disease than are MM or VV individuals .

Monday, 21 May 2018

1.9 million brain #cells are destroyed every minute after a stroke

Here’s how much stroke would be reduced if each were eliminated:

#Hypertension 47.9%

Physical inactivity 35.8%

Lipids (blood fats) 26.8%

Poor diet 23.2%

Obesity 18.6%

#Smoking 12.4%

#Heart causes 9.1%

#Alcohol intake 5.8%

#Stress 5.8%

#Diabetes 3.9%

Learn more facts presented in live at : https://bit.ly/2uelcLc