Sunday, December 4, 2011

Cotinine for Alzheimer's Treatment

A compound derived from tobacco, cotinine, reduced beta-amyloid plaque aggregation in the brain's of mice with the Alzheimer's disease model. The treated mice also performed better on tasks measuring working memory.
Journal of Alzheimer's Disease online Feb 14 2011

Intractable Pain Treatment

Investigators conducted a phase 1 trial of intradermal NP2, a novel gene transfer vector, which was found to be safe and well tolerated for the treatment of intractable pain resulting in pain relief in cancer patients who were unresponsive to morphine or other treatments.
Annals of Neurology online April 2011

Drosophila Model for Alzheimer's Disease

Joshua Shulman,MD,PhD , instructor of neurology at Harvard medical school used the drosophila model for Alzheimer's disease to determine how variants function. The drosophila tauopathy model, which exhibits age-dependent neurodegeneration, decreased lifespan and hyperphophorylated and misfiled tau protein. The model is used to functionally screen candidate genes in AD which may lead to sooner treatment options for afflicted patients.
Arch Neurol 2011; E-Pub Sept 12 2011

Low Vitamin D and Sleepiness/Muscle Pain

Osteomalacic myopathy (diffuse muscle pain) can interfere with sleep quality and contribute to daytime drowsiness. Patients found to have 25-OH vitamin D < 30 ng/mL were treated. 81 0f 153 patients responded positively to vitamin D3 replacement.
J Clin Sleep Med, 2010; 6 (6): 605-608
Med Hypotheses. 2011 ; 76 (2) :208-213

ALS/FTD Major New Gene Discovery

The gene , called chromosome 9 open reading frame 72 (C9ORF72), contributes to 40% of familial (inherited) and 7-10% of sporadic (non-inherited) ALS and is linked to a seemingly unrelated neurodegenerative disorder (but known to be associated with ALS) Frontotemporal Degeneration (dementia).The function of the gene is as yet unknown. This mutant gene causes a toxic build-up of RNA .
C9ORF72 can be traced back to a "founder" person in Scandinavia 1500 years ago! This discovery prompts investigators to question whether there is actually a "sporadic" form of ALS, given that careful investigation of such patients may in fact reveal a relative with FTD.
NEURON 2011; E-pub Sept 21 2011

Wednesday, September 7, 2011

Alzheimer's Plaque Origin : Amyloid plaques may originate in the liver, not the brain

Higher expression of presenilin 2in the liver correlated with greater accumulation of Beta-amyloid in the brain and the development of Alzheimer's disease suggesting that blocking amyloid production in the liver may protect the brain.
Journal of Neuroscience Research March 3 online

Recurrent Stroke Risk Cut With Statins Even in Those Without Diabetes

Statin therapy appears to reduce the risk of recurrent stroke among patients with diabetes or the metabolic syndrome to the same degree that it does in patients who have neither disorder, according to a planned post hoc analysis of data collected in the Stroke Prevention by Aggressive Reduction in Cholesterol Levels clinical trial (SPARCL).

Metabolic Dysfunction LInked to Cyclic Vomiting Syndrome

About a third of children with cyclic vomiting syndrome appear to have some metabolic condition, either mitochondrial dysfunction, fatty acid oxidation dysfunction, or a combination of both. According to Dr. David Rothner at the Cleveland Clinic in a largest-to-date case series of metabolic testing in patients with CVS presented at the American Headache society meeting in Washington.

Tuesday, September 6, 2011

That Itches

It is reported that 17 % of adults suffer from chronic itch. Zhou-Feng Chen , of WUSOM , and his team have discovered an itch receptor called GRPR and itch specific neurons. Itch receptors are located not just in the skin but also in the brain and spinal cord.
How does this complex system work ? Stay tuned...


Feinberg School scientists found the cause of ALS by discovering a protein, ubiquilin2, whose critical job is to recycle damaged or misfolded proteins in motor and cortical neurons and shuttle them off to be reprocessed. In people with ALS, Feinberg researchers found ubiquilin2 isn’t doing its job. As a result, the damaged proteins and ubiquilin2 loiter and accumulate in the motor neurons in the spinal cord and cortical and hippocampal neurons in the brain. The protein accumulations resemble twisted skeins of yarn -- characteristic of ALS -- and cause the degeneration of the neurons. Researchers found ubiquilin2 in these skein-like accumulations in the spinal cords of ALS cases and in the brains of ALS/dementia cases.

Wednesday, July 27, 2011

New Alzheimer's Biomarker

Researchers found that the best predictor of whether someone would develop Alzheimer’s disease was a combination of cerebrospinal fluid sAPP (soluble amyloid precursor protein ), CSF tau protein (an established marker of brain cell damage) and the age of the individual. When these factors were combined, the results were roughly 80 percent accurate in predicting whether the disease would develop.

The protein amyloid beta1-42, or A1-42, which has previously been considered a CSF biomarker for Alzheimer’s disease, was not a predictive factor in this study.

Tuesday, July 26, 2011

Traumatic Brain Injury identified by serum Biomarker

Glial fibrillary acidic protein (GFAP) is found in glial cells and is specific to the central nervous system.
Currently the Glasgow Coma Scale(GCS) is the primary measure used to assess patients with head injury, but it can be influenced by intoxicants, medicine, other injuries, or hypo perfusion.
Patients in a study at the Orlando Regional Medical center that presented with traumatic brain injury had blood collected within 4 hours of injury.
Early GFAP levels were able to distinguish TBI patients from normal controls and differentiated those with mild TBI (GCS15).
These findings may guide emergency medical physicians in the evaluation and treatment of patients presenting with altered sensorium.

Monday, May 30, 2011

Safinamide for Parkinson's Dyskinesia

Safinamide has been shown in animal models to inhibit glutamate release. Levadopa treatment is believed to cause glutamate release. Studies in primates show that levadopa-induced dyskinesia can be blocked by safinamide.
In a study of 214 patients with PD and dyskinesia, those that received 100 mg/d of safinamide experienced a reduction of 24 % compared to placebo.
AAN 2011 annual meeting

Tinnitus Treatment

University of Texas, Dallas researcher Navzer Engineer,PhD.reversed the physiological and behavioral correlates of tinnitus in noise-exposed rats by pairing a range of tone frequencies with peripheral nerve stimulation of the vagus nerve.
Nature 2011; 470:101-4

Parkinson's and Pesticides

University of Colorado investigators have found that higher concentrations of four pesticides - simazine, atrazine, metachlor and alachlor - in groundwater increases PD risk. For every 10 mcg/L increase of pesticide levels in drinking water the risk for PD increased by 3%. Samples they obtained ranged from 0.0005 - 20 mcg/L.
This study follows from W. Langston's discovery of a bad batch of heroin that had been contaminated with a neurotoxin MPTP that lead to an outbreak of individuals with a Parkinson's disease-like symptom complex. MPP+ is the toxic metabolite of MPTP and is very similar to paraquat, one of the most widely used herbicides in the world. To date, there have been over 50 studies linking pesticides/herbicides with PD.

Monday, May 16, 2011

New Oral MS Drug Reduces Relapses

Oral Laquinimod reduced MS relapses by 23% in phase III trial as reported by Giancarlo Comi at the AAN meeting in Hawaii. Most importantly, Laquinimod reduced cerebral atrophy by 33%. The drugs novel mechanism of action addresses inflammatory activity and accumulation of irreversible tissue damage. Also importantly the side effect was low especially compared to fingolimod (Gilenya) released this past year. Teva produces Laquinimod

Saturday, April 23, 2011

Parkinson's and Protein Kinase Pathway

NIH researchers have found a pathway that regulates production of kinase-C. By modifying p300, researchers can possibly reduce the expression of kinase-C and the associated destructive effects on dopamine-producing cells. Next.... to find the chemicals to control the mechanism.....
Jrnl of Neuroscience 2/9/11

Stroke, Atrial Fib And Dementia

Patients with atrial fibrillation that have had stroke are 2.4 times more likely to develop dementia.
Neurology March 8 2011

Monday, April 11, 2011

Diet soda and Stroke risk

Researchers observe an increased risk of vascular disease , including heart attack and stroke, in those who drink diet soda daily.
Am J Clin Nutr. 2009;89(4):1037-1042

Tobacco Use and ALS

The risk of developing ALS increases 44% for former smokers and 42% for current smokers, compared with those who have never smoked.
Arch Neurol.2011;68(2)207-213

Hearing Loss and Dementia

Hearing loss is linked to dementia in individuals older than 60. Hearing loss may be causally related to dementia, maybe through exhaustion of cognitive reserve, social isolation, environmental differentiation, or a combo of these.
One wonders if the use of digital hearing aids, cochlear implants, or other rehabilitative strategies to treat hearing loss would result in a decreased risk for dementing illness.
Arch Neurol. 2011 ; 68(2):207-213

Sunday, April 10, 2011

Cell Phones Increase Brain Metabolism

Cell phone use increases brain glucose metabolism in the region closest to the antennae as per a JAMA article of February 23rd.Whether these changes are due to heat generated by the phone or RF-EMF exposure is unclear. The significance of this finding is also unclear. Researchers are divided about the risk of brain cancer and cell phone use. Some researchers have also suggested a neuro-protective effect that exposure to electromagnetic waves in mice decreases the accumulation of amyloid in mice (the protein found in excess in the brains of those with Alzheimer's) J Alzheimer's Dis 2010;19(1):191-210

Dysphasia : TIA vs Complicated Migraine

Serene Branson while reporting live at the Grammy Awards suddenly began having difficulty speaking.She was hospitalized at UCLA Medical Center in LA and after a neurologic workup was diagnosed with migraine.She had no prior history of migraine and recovered completely.
Another TIA mimic may be related to seizures. For example, following a seizure , some patients may experience sided paralysis called Todd's paralysis which resolves without sequelae.
To aid the physician in diagnosis the ABCD2 algorithm score based on age, blood pressure, clinical features, a history of diabetes and TIA duration can predict stroke risk.
A prior history of unexplained transient neurologic attacks, the presence of non- specific symptoms, and gradual symptom onset can help differentiate between TIA and TIA mimics such as migraine.
With migraine, symptoms occur over minutes. In TIA's over seconds.
With TIA mimics, patients often report other non-focal symptoms such as lightheadedness, GI complaints and tightness of the chest.
In 2010, the American Stroke Association revised diagnostic criteria for TIA.
All of the aforementioned can assist the physician in making a correct diagnosis and most importantly identify those at risk for stroke.
AHA/ASA Guidelines for the prevention of stroke in patients with TIA's ( Stroke 2011; 42: 227-276)