2009 IoN News Archive
- Grant for research into new epilepsy treatments
- Professor Martin Rossor has been recognised by the The Alzheimer's Association
- Drug discovery collaboration on inclusion body myositis
- PDS awards Training Fellowship to Institute of Neurology researcher to understand how the brain controls Parkinson’s symptoms
- Alan Thompson to lead UCL Partners Neurological Disorders theme
- World MS Day - Wednesday 27th May - Global initiative to highlight Multiple Sclerosis
- Queen Square leads on new UK recommendations for bladder management which can dramatically improve quality of life in Multiple Sclerosis
- John Hardy most-cited Alzheimer's disease researcher in the UK
- Prestigious awards for Institute researchers
- Drug study offers hope for Alzheimer’s treatment
- Brain activity predicts our choices
- Professor George du Boulay CBE, FRCR, FRCP
- Brain awareness week: the impact of UCL research
- Parkinson's-linked mutation makes neurons vulnerable to calcium-induced death
- Second round of NIHR Senior Investigators announced
- 'Mind-Reading' Experiment Highlights How Brain Records Memories
- Anti-malaria drug does not appear to help with human prion diseases.
- UCL Partners is one of UK’s first Academic Health Science Centres
- "Opening doors for patients with MS"
- Are we as decisive as we think?
- "Magnets stop the nightmare of tinnitus, researchers say."
- Prestigious award for Professor Hugh Bostock
- Untangling the Brain
- Young UCL Investigator Award in neuroimaging techniques
- Brain disease "resistance gene" could offer insights into CJD
- Neurology: A Queen Square Textbook
- Headache: annual evidence update
- Roads closed for powerful MRI scanner delivery
- Long-term risks lower for surgical treatment of carotid stenosis
- Memorandum of collaboration signed
- Professor John Hardy joins the ranks of science greats
- Drug study offers hope for Alzheimer's treatment
- Prestigious award for Professor David Miller
- Magnets stop the nightmare of tinnitus, researchers say.
- Brain activity predicts our choices
- Jon Driver Award
- Professor Sander named recipient of the American Epilepsy Society 2009 Clinical Science Award
- Study highlights effect of brain waves on human behaviour
- New podcast describes the significance and impact of highly cited paper
- NIH Grant for research into inherited neuropathies
- How the brain knows a dog is a dog: concept acquisition in the human brain
- Prof Elizabeth Fisher elected member of the European Molecular Biology Organization (EMBO)
- Locating literacy in the brain
- Dopamine enhances expectation of pleasure in humans
- Queen Square scientists question memory theory
- IoN scientist to front Alzheimer’s Research Trust national appeal
- New doors open to the understanding of the origin of brain tumours
Published: Jul 8, 2013 2:00:00 PM
Published: Jul 5, 2013 5:29:00 PM
Neurodevelopmental, neurodegenerative and neuromuscular disorders associated with defective autophagy
Published: Jun 18, 2013 4:38:00 PM
Published: Jun 10, 2013 4:35:00 PM
Untangling the Brain
26 January 2009
Younger brains better than old in clearing Alzheimer’s-related protein, study finds. Younger brains are more effective than older brains at getting rid of abnormal amounts of tau protein associated with Alzheimer’s disease – a mechanism that may be partly explained by a better stress response in the young, a mouse-model study led by researchers at the University of South Florida found.
The study, published this month in the American Journal of Pathology, also suggests that once some abnormal tau is produced in the brain it may interfere with the normal turnover of tau protein and lead to its destructive buildup. While normal tau helps maintain the structure of neurons, the excessive accumulation of tau leads to fibrous Alzheimer’s tangles that choke the brain’s memory center.
" The accumulation of abnormal aggregates of tau (tangles) is a feature not
only of the Alzheimer's disease brain but also in the other "tauopathies" which
include the parkinsonian disorder, progressive supranuclear palsy
This study shows that a small amount of abnormal tau can act as a "seed" for facilitating the conversion of normal tau, leading to functional impairment and accumulation.
In the normal human brain, tau is present as 6 closely related variants and each of these variants may have a distinct function. There is increasing evidence that the composition of tau related to these six variants is finely balanced and that subtle changes in one or more of these variants can cause damage and death of specific neuronal populations. In our lab, we have shown that even without overt mutational defects in the tau protein, common genetic variation in the tau gene can cause such subtle changes in the levels and ratios of the 6 tau variants and increase risk of PSP. The findings in this paper show that the presence or excess of one defective variant of tau could impair clearance of "normal" tau thereby inducing a cascade of deleterious changes."
read more >> insciences.org
reference >> American
Journal of Pathology. 2009; 174: 228-238.). DOI: