Friday, 20 April 2018


PRIMARY AGE-RELATED TAUOPATHY

A neurological disease in people that have symptoms similar to Alzheimer’s disease, but lack the amyloid plaque in the brain that is considered a hallmark of that disease.

The newly coined disease is called primary age-related tauopathy (PART). Patients with PART have symptoms of cognitive impairment synonymous with Alzheimer’s, but only have another type of protein in the brain called tau that can contribute to memory loss when it malfunctions.

Recent diagnostic tests and biomarkers found in cerebral spinal fluid indicate that a large percentage of patients with mild cognitive impairment — as high as 25% in some studies — may have PART considering they have tau protein but no amyloid.

To explore your ideas on PART, click here

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Thursday, 19 April 2018



Deep brain stimulation involves implanting electrodes within certain areas of your brain. These electrodes produce electrical impulses that regulate abnormal impulses. Or, the electrical impulses can affect certain cells and chemicals within the brain.

The amount of stimulation in deep brain stimulation is controlled by a pacemaker-like device placed under the skin in your upper chest. A wire that travels under your skin connects this device to the electrodes in your brain.

Deep brain stimulation is used to treat a number of neurological conditions, such as:

Ø  Essential tremor
Ø  Dystonia
Ø  Epilepsy
Ø  Chronic pain
Ø  Obsessive compulsive disorder

Deep brain stimulation is also an experimental treatment for major depression, stroke recovery, addiction and dementia.

Results

Deep brain stimulation won't cure your disease, but it may help lessen your symptoms. If deep brain stimulation works, your symptoms will improve significantly, but they usually don't go away completely. In some cases, medications may still be needed for certain conditions. Deep brain stimulation isn't successful for everyone.

Interested to explore your ideas on Deep brain stimulation, click here

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Wednesday, 18 April 2018



MDD, also referred to as clinical depression, is a significant medical condition that can affect many areas of your life. It impacts mood and behavior as well as various physical functions, such as appetite and sleep.
MDD is one of the most common mental disorders in the United States. In 2015, nearly 7 percent of Americans over age 18 had an episode of MDD.


Symptoms

Ø  Feeling sad or irritable
Ø  Less interested in activities you once enjoyed.
Ø  Lose or gain weight or a change in appetite.
Ø  Sleeping more than usual.
Ø  Restlessness.
Ø  Feeling tired and a lack of energy.


Causes

The exact cause of MDD isn’t known. However, there are several factors that can increase the risk of developing the condition. A combination of genes and stress can affect brain chemistry and reduce the ability to maintain mood stability. Changes in the balance of hormones might also contribute to the development of MDD.

MDD may also be trigged by:

·         Alcohol or drug abuse
·         Certain medical conditions, such as cancer or hypothyroidism

Treatment

o   Medication by prescribing antidepressant medications such as fluoxetine (Prozac) and citalopram (Celexa).
o   Psychotherapy
o   Changes in Lifestyle

Interested to explore your ideas on MDD, click here

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Friday, 13 April 2018

Keynote Talk on Electrographic Seizures and Encephalopathy


KEYNORE TALK
Title : Electrographic Seizures in Pediatric Systemic Cancer Patients with acute Unexplained Encephalopathy Diagnostic role of Bedside Emergent ≥ 30min EEG
Author : Muhammad Akbar Malik
               Top-Down-Bottom-Up
               Pakistan
Abstract:
Statement of the Problem: Systemic pediatric cancer patients are prone to become critically ill and may develop seizures and encephalopathy, which can result in permanent neurologic disability. There are few techniques for monitoring brain functions in these patients, especially in resource-poor settings. The emergent bed-side electroencephalogram (EEG) can be useful.
Purpose: to determine, usefulness of emergent bedside EEG features among these patients with unexplained coma (GCS≤8) of ≤6 hrs duration. 
Methodology & Theoretical Orientation: Prospective EEG assessment of 40 systemic cancer patients consecutively diagnosed and admitted in neurointensive care units. Patients with brain tumor, brain metastasis, seizures or those with known cause of coma were excluded. 
Findings: Over a period of 2 year, 40 children; boys 65% and girls 35%, with systemic cancer patients with a median age of 9.8 years were studied. This cohort underwent bed-side EEG of ≥ 30 minutes, which was abnormal in 100% of the records. The most common EEG abnormalities were invariant mixed theta-delta slowing (27.5%), followed by low-amplitude delta pattern plus epileptiform discharges (20%) and there was electrographic evidence of EEG seizures in 17(42.5%) of the cohort. These electrographic seizures were present in 55.5% of 18 patients with subtle convulsions, whereas were documented only in 20% of the 22 patients without such movements. Electrographic seizures among patients with subtle convulsions responded to anticonvulsant drugs in 75% cases as compared 50% such response among patients without such convulsions. 
Conclusion& Significance: Seizures are common among critically ill children with systemic cancer. Bed-side EEG record of ≥30 minutes is useful in such patients. Recommendations are made for emergent ≥ 30min EEG among systemic cancer patients with unexplained acute coma.

Wednesday, 11 April 2018


ORAL PRESENTATION
Title Dual Activity of PAC: Neurotrophicity and Neuroprotection against  amyloid peptides causing Alzheimer’s disease
Author : Fadia El Bitar
               King Faisal Specialist Hospital and Research Centre, Saudi Arabia
Abstract : Alzheimer’s disease (AD) is the most common cause of dementia in the elderly. The toxicity of -amyloid (A) peptides is thought to be involved in neuronal damage in this pathology. Multiple studies focused on role of neuroprotective molecules to attenuate the toxic consequences of A peptides in the development of AD.
       In the present work, our objective is to investigate in vitro if PAC which is the synthetic analogue of curcumin displays #neuroprotective activity against A peptide-induced #neurotoxicity, using rat neuroblastoma B104 as cell culture model. Our results showed that PAC is not neurotoxic per se. In addition, PAC showed a striking #neurotrophic activity in cells cultured at low density. This neuronal outgrowth increases importantly with increasing days of culture starting from 2 folds increase at day 2 to 3 folds increase at day 5. The number of neurites per cell rises also in presence of PAC.
       Most importantly, we demonstrate the capacity of PAC to correct sA25-35 neurotoxicity. The percentage of cell viability increases significantly by PAC at 0.5µM in presence of sA 25-35 compared to that in presence of the peptide alone .Interestingly, our neurotrophic and neuroprotection studies showed the PAC was 20 times more efficient than curcumin. Both PAC and curcumin displayed an effect on cell-cell interaction.
       Thus, our results revealed neuroprotective properties of PAC against A peptide. The continuity in examining the mechanism(s) underlying PAC activity is promising towards identifying efficient therapy for AD.

Tuesday, 10 April 2018


POSTER PRESENTATION

TitleDifferential Expression of the Insulin Receptor in Primary Sensory Neurons Innervating Somatic and Visceral Organs

Author : Bence Andras Lazar 
                University of Szeged, Hungary

Abstract In recent years, several studies indicated functional interactions between the insulin receptor (InsR) and the transient receptor potential vanilloid type 1 receptor (TRPV1) co-expressed in a subset of primary sensory #neurons (PSNs) of unidentified target innervation. The aim of the present study was to reveal the target-specific expression of the InsR and its co-localization with TRPV1 in adult rats. Adult male Wistar rats (n=12) weighing 300-350 g were used. To identify somatic and visceral PSNs biotin-conjugated wheat germ agglutinin (bWGA) was injected into the hind paw skin, the lateral gastrocnemius muscle, the pancreas and the urinary bladder. Three days later representative serial sections were cut from Th10-13 and L3-Sdorsal root ganglia. Immunohistochemistry and quantitative morphometry were used to analyze the expression of InsR and TRPV1 in bWGA-labelled somatic and visceral PSNs. The largest proportions of retrogradely labelled InsR-positive neurons were identified among PSNs serving the pancreas (~54%) and the urinary bladder (~52%). InsR-positive neurons innervating the hind paw skin and the gastrocnemius muscle amounted to ~22% and ~21% of labelled neurons. The majority (~64%) of the labelled PSNs exhibited TRPV1 immunoreactivity. Co-localization of the TRPV1 and the InsR was observed in ~16%, ~15%, ~29% and ~30% of labelled cutaneous, muscular, pancreatic and urinary bladder PSNs. Our quantitative morphological data provide evidence for the co-localization of InsR and TRPV1 in PSNs innervating somatic and visceral organs and demonstrate a preponderance of InsR-immunoreactivity among PSNs which innervate visceral targets. These findings suggest that visceral spinal PSNs might be more sensitive to the modulatory influence of insulin than PSNs innervating somatic organs.

Keywords: insulin receptor; transient receptor potential vanilloid type 1 receptor; primary sensory neurons; retrograde labelling; somatic and visceral organs. 



Study Finds That, Low Dopamine Levels May Mean Increased Risk of Alzheimer's Disease!!

Highly sensitive MRI scans revealed a potential link between dopamine and a part of the brain that may impact the future of Alzheimer’s diagnosis. 

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