Just wanna say thank you! :D Your blog inspires me to write more about science. Keep up the great work and promote science!
Thank you for following this blog and your kind words :]
July 2011
8 posts
“Within psychology and neuroscience, some new and rigorous experimental paradigms for studying consciousness have helped it begin to overcome the stigma that has been attached to the topic for most of this century.”
—David Chalmers, a philosopher specializing in philosophy of the mind and consciousness
June 2011
12 posts
Looking for a neuroscience graduate program that's right for you? Click here! →
graduate-school.phds.org
Hi guys,
This is something I found while I was replying privately to one of the many questions you guys send me. In this case, somebody was asking about finding programs that were a good fit… I tried this site and was pleased with the results… Basically, it’s a simple online tool that ranks neuroscience/neurobiology graduate schools according to the characteristics you want in a program.
Hope you like,
M.
You have no idea how much I love you for posting the GABA stuff. I'm doing a neurochemistry assignment at the moment specifically related to GABA and Glutamate. The post was a big help, so thank you!
Thanks :] I made a similar one about glutamate. You can find it here: http://houseofmind.tumblr.com/post/3710353507/up-next-in-the-neurotransmitter
I just read your reblog about Huntington's and I was wondering... is adult onset Huntington’s just suddenly triggered at a certain age (with the approrpriate number of repeats in their genome since birth) or are the repeated segments repeated in replication errors until the number of tandem repeats triggers the disease?
Hey,
Great question! I’ve been searching online and can’t arrive at a solid answer. I personally don’t know, but from what I’ve read I think it’s the number of tandem repeats that triggers the disease… For example, people with +40 tandem repeats usually develop the disease while people with 36-40 repeats may or may not develop the disease.
Here’s the link I found useful: http://ghr.nlm.nih.gov/condition/huntington-disease
Daily Diseases and Disorders: Huntington's Disease →
dailydiseasesanddisorders.tumblr.com
Huntington’s disease is a neurodegenerative genetic disorder that greatly affects muscle coordination and cognition. The nerve cells in the brain slowly breakdown and atrophy. Huntington’s disease affects the striatum of the brain as well as the hippocampus, purkinje cells, and the cerebellum.
Huntington’s is an autosomal dominant genetic disease that results from a defect on chromosome #4. The defect causes a repeat in a CAG sequence on the DNA to occur many more times than normal. In person without Huntington’s, the CAG sequence is repeated 10 to 35 times. In an individual with Huntington’s disease, the repeat can be repeated 36-120 times. The repeated sequence is expanded as it is passed through one generation to the next, lengthening the sequence in each offspring. Therefore, the disease becomes progressively juvenile. If one parent has Huntington’s, the child has a 50% chance of having the disease as well.
There are two types of Huntington’s: juvenile which appears in children and the much more common form, adult-onset Huntington’s which appears in an individual aged 30 to 40.
Huntington’s disease has become a target due to the ethical issues associated with it. Many question when an individual should be tested for the disease, if at all. Preimplantation genetic diagnosis has been used as a selective form of abortion. Some individuals who might have the disease may opt to not have the disease diagnosed.
Worldwide, 5-10 people out of 100,000 have the disease.
After the first onset of symptoms, an individual typically has a life span of twenty more years of life. Huntington’s has no cure and ultimately leads to death. Suicide is one of the greatest cause of fatalies in the disease with 7.3% with Huntington’s taking their own lives and up to 27% attempting suicide.
Diagnosis: A genetic counselor can determine if the child will have Huntington’s disease using genetic testing. The geneticist will look at the number of CAG repeats and determine the likelihood of the person developing Huntington’s in their life. In most cases, the affected individual will have an idea of when the symptoms will onset. A physical diagnosis that analyzes the symptoms of Huntington’s is also effective for most patients. Medical imaging of the brain can also show which areas of the brain have atrophied.
Symptoms: Huntington’s disease affects many parts of the body. Movement disorders can include involuntary jerking, sustained contraction of muscles, rigidity, diffulty with speech, posture problems, and difficulty swallowing. Cognitive disorders include difficulty with organization, emotional flexibility, lack of focus and reasonable thinking, and various other symptoms. Lastly, psychiatric disorders include sadness, unhappiness, social withdrawal, loss of interest, fatigue, feelings of guilt, reduced appetite, and reduced sex drive.
Treatment: There is no cure for Huntington’s disease. Some of the symptoms can be controlled with various antidepressants and other drugs that reduce the amount of involuntary muscle jerking.
Additional Information: Huntington’s disease has become prominent in different media sources and has appeared in Everwood, House, Private Practice, ER, and Scrubs.
Hi!
Can you tell me the difference between Psychophysiology, cognitive neuroscience, and neuropsychology? I know they are closely related, but are the interchangeable or quite distinct?
I personally don’t consider them interchangeable.
As far as I’m concerned, psychophysiology is a branch within psychology interested in the physiological processes that underlie psychological processes, although on a very basic (uncomplicated) level. To add to the confusion, people use interchangeable terms like psychobiology, biopsychology and physiological psychology as well. These are pretty much equivalent.
Cognitive neuroscience is a branch of psychophysiology that encompasses more concrete (i.e. scientific) knowledge from other disciplines (neuroscience) and is more specifically related to cognition, cognitive function and the role of brain function in these processes.
Neuropsychology on the other hand, is more thorough (IMO) because it focuses on the neural bases of the brain’s structure and function in relation to specific behaviors (which may or may not be related to pathology) and other psychological processes. Neuropsychology is also more closely tied to pathology and figuring out what’s wrong in the brain or nervous system and how to fix it…
Just thought I would let you know your blog's really interesting and I wish I knew about it sooner. Keep up the good work :)
Cheers
Thanks :)
“Swiftly the brain becomes an enchanted loom, where millions of flashing shuttles weave a dissolving pattern-always a meaningful pattern- though never an abiding one.”
—Charles Sherrington (Nobel Prize winner in Physiology and Medicine, 1953)
May 2011
17 posts
Potential New Drug Candidate Found for Alzheimer’s Disease →
health.ucsd.edu
Researchers at the University of California, San Diego, the Medical University of South Carolina and American Life Science Pharmaceuticals of San Diego have demonstrated that oral administration of a cysteine protease inhibitor, E64d, not only reduces the build-up of β-amyloid (Aβ) in the brains of animal models for Alzheimer’s disease, but also results in a substantial improvement in memory deficit. (More here)
From the news release:
Increased Aβ levels in the brain are associated with the development of memory loss and amyloid plaque, the hallmark of Alzheimer’s disease. Aβ peptides are “cut” out from a larger protein called the amyloid precursor protein (APP) by an enzymatic “scissor” called β-secretase, and aggregate to form plaques in the brain regions responsible for memory.
E64d reduces Aβ by inhibiting the β-secretase “scissors” from “cutting” the APP chain into smaller toxic Aβ peptides. But in this study, the researchers found that the compound actually increases the activity of a protease called BACE1 which, to date, has been regarded as the primary β-secretase. Instead, E64d appears to lower brain Aβ by inhibiting the β-secretase activity of another protease, Cathepsin B.
