Skip to main content

Home/ SciByte/ Group items tagged Alzheimer

Rss Feed Group items tagged

Filter: All | Bookmarks | Topics Simple Middle
Mars Base

New drug reverses loss of brain connections in Alzheimer's disease - 0 views

medicalxpress.com/...rses-loss-brain-alzheimer.html

scibyte99 Alzheimer

shared by Mars Base on 18 Jun 13 - No Cached
  • The first experimental drug to boost brain synapses lost in Alzheimer's disease
  • combines two FDA-approved medicines to stop the destructive cascade of changes in the brain that destroys the connections between neurons, leading to memory loss and cognitive decline.
  • The decade-long study
  • ...21 more annotations...
  • shows that NitroMemantine can restore synapses, representing the connections between nerve cells (neurons) that have been lost during the progression of Alzheimer's in the brain
  • These findings actually mean that you might be able to intercede not only early but also a bit later
  • Alzheimer's patient may be able to have synaptic connections restored even with plaques and tangles already in his or her brain.
  • study, conducted in animal models as well as brain cells derived from human stem cells,
  • team mapped the pathway that leads to synaptic damage in Alzheimer
  • found that amyloid beta peptides, which were once thought to injure synapses directly
  • actually induce the release of excessive amounts of the neurotransmitter glutamate from brain cells called astrocytes that are located adjacent to the nerve cells.
  • Normal levels of glutamate promote memory and learning, but excessive levels are harmful
  • Alzheimer's disease, excessive glutamate activates extrasynaptic receptors, designated eNMDA receptors
  • which get hyperactivated and in turn lead to synaptic loss
  • lab had previously discovered how a drug called memantine can be targeted to eNMDA receptors to slow the hyperactivity seen in Alzheimer's.
  • memantine's effectiveness has been limited.
  • memantine—a positively charged molecule—is repelled by a similar charge inside diseased neurons
  • memantine gets repelled from its intended eNMDA receptor target on the neuronal surface.
  • FDA approval of memantine in 2003
  • a fragment of the molecule nitroglycerin—a second FDA-approved drug commonly used to treat episodes of chest pain or angina in people with coronary heart disease—could bind to another site that the Lipton group discovered on NMDA receptors.
  • memantine rather selectively binds to eNMDA receptors, it also functions to target nitroglycerin to the receptor
  • by combining the two, Lipton's lab created a new, dual-function drug
  • researchers developed 37 derivatives of the combined drug before they found one that worked
  • By shutting down hyperactive eNMDA receptors on diseased neurons, NitroMemantine restores synapses between those neurons
  • NitroMemantine brings the number of synapses all the way back to normal within a few months of treatment in mouse models of Alzheimer's disease. In fact, the new drug really starts to work within hours
Mars Base

Study unravels central mystery of Alzheimer's disease - 0 views

medicalxpress.com/...mystery-alzheimer-disease.html

scibyte90 Alzheimer

shared by Mars Base on 11 Apr 13 - No Cached
  • Until recently, Polleux's laboratory has been focused not on Alzheimer's research but on the normal development and growth of neurons
  • In 2011
  • reported that AMPK overactivation by metformin, among other compounds, in animal models impaired the ability of neurons to grow output stalks, or axons
  • ...25 more annotations...
  • Around the same time, separate research groups found clues that AMPK might also have a role in Alzheimer's disease
  • One group reported that AMPK can be activated in neurons by amyloid beta, which in turn can cause a modification of the protein tau in a process known as phosphorylation
  • a postdoctoral research associate
  • began by confirming that amyloid beta, in the small-aggregate ("oligomer") form that is toxic to synapses, does indeed strongly activate AMPK
  • amyloid beta oligomers stimulate certain neuronal receptors, which in turn causes an influx of calcium ions into the neurons
  • that this calcium influx triggers the activation of an enzyme called CAMKK2, which appears to be the main activator of AMPK in neurons
  • AMPK overactivation in neurons is the essential reason for amyloid beta's synapse-harming effect
  • neurons' dendritic spines—the rootlike, synapse-bearing input stalks that receive signals from other neurons
  • scientists showed that amyloid beta oligomers can't cause this dendritic spine loss unless AMPK overactivation occurs—and indeed AMPK overactivation on its own can cause the spine loss
  • the team used J20 mice, which are genetically engineered to overproduce mutant amyloid beta
  • when we blocked the activity of CAMKK2 or AMPK in these neurons, we completely prevented the spine loss
  • Recent studies have shown that amyloid beta's toxicity to dendritic spines depends largely on the presence of tau, but just how the two Alzheimer's proteins interact has been unclear
  • their colleagues are now following up with further experiments to determine what other toxic processes, such as excessive autophagy, are promoted by AMPK overactivation and might also contribute to the long-term aspects of Alzheimer's disease progression
  • also interested in the long-term effects of blocking AMPK overactivation in the J20 mouse model as well as in other mouse models of Alzheimer's disease, which normally develop cognitive deficits at later stages
  • the pharmaceuticals industry who are potentially interested in targeting either CAMKK2 or AMPK
  • show that brain damage in Alzheimer's disease is linked to the overactivation of an enzyme called AMPK
  • Researchers have known for years that people in the earliest stages of Alzheimer's disease begin to lose synapses in certain memory-related brain areas
  • findings, reported in the April
  • Small aggregates of the protein amyloid beta can cause this
  • but how they do so has been a mystery
  • Tangles of tau with multiple phosphorylations ("hyperphosphorylated" tau) are known to accumulate in neurons in affected brain areas in Alzheimer
  • investigate further, to determine whether the reported interactions of AMPK with amyloid beta and tau can in fact cause the damage seen in the brains of Alzheimer's patients
  • In addition
  • findings suggest the need for further safety studies on an existing drug, metformin.
  • , a popular treatment for Type 2 Diabetes, causes AMPK activation.
Mars Base

U.S. FDA Approves Possible Alzheimer's Test - ScienceInsider - 0 views

news.sciencemag.org/...roves-possible-alzheimers.html

scibyte42 Alzheimer

shared by Mars Base on 12 Apr 12 - No Cached
  • the U.S. Food and Drug Administration (FDA) approved a radioactive compound for evaluating people with cognitive impairment for Alzheimer's disease
  • Amyvid, binds to amyloid plaques, the calling card of Alzheimer's disease in the brain
  • before a PET scan, Amyvid allows doctors to see whether amyloid has begun to build up
  • ...6 more annotations...
  • negative test reduces the likelihood
  • a positive test does not necessarily confirm
  • concerns: that it could be overused in general
  • and there will be
  • both false positives and false negatives
  • medical community is going to have to develop its own standards
Mars Base

Green tea and red wine extracts interrupt Alzheimer's disease pathway in cells - 0 views

medicalxpress.com/...en-tea-red-wine-alzheimer.html

scibyte81 Alzheimer

shared by Mars Base on 06 Feb 13 - No Cached
  • Natural chemicals found in green tea and red wine may disrupt a key step of the Alzheimer's disease pathway
  • Alzheimer's disease is characterised by a distinct build-up of amyloid protein in the brain
  • clumps together to form toxic, sticky balls of varying shapes
  • ...10 more annotations...
  • These amyloid balls latch on to the surface of nerve cells in the brain by attaching to proteins on the cell surface called prions
  • investigate whether the precise shape of the amyloid balls is essential for them to attach to the prion receptors
  • if so, we wanted to see if we could prevent the amyloid balls binding to prion by altering their shape, as this would stop the cells from dying
  • The team formed amyloid balls in a test tube and added them to human and animal brain cells
  • When we added the extracts from red wine and green tea, which recent research has shown to re-shape amyloid proteins, the amyloid balls no longer harmed the nerve cells
  • this was because their shape was distorted, so they could no longer bind to prion and disrupt cell function
  • showed, for the first time, that when amyloid balls stick to prion, it triggers the production of even more amyloid
  • the team's next steps are to understand exactly how the amyloid-prion interaction kills off neurons
  • that this will increase our understanding of Alzheimer's disease even further, with the potential to reveal yet more drug targets,
  • While these early-stage results should not be a signal for people to stock up on green tea and red wine, they could provide an important new lead in the search for new and effective treatments
Mars Base

Prospective Alzheimer's drug builds new brain cell connections - 0 views

medicalxpress.com/...alzheimer-drug-brain-cell.html

scibyte67 Alzheimer

shared by Mars Base on 11 Oct 12 - No Cached
  • researchers have developed a new drug candidate that dramatically improves the cognitive function of rats with Alzheimer's-like mental impairment
  • intended to repair brain damage that has already occurred
  • This is about recovering function
  • ...20 more annotations...
  • t makes these things totally unique. They're not designed necessarily to stop anything. They're designed to fix what's broken. As far as we can see, they work
  • current Alzheimer's treatments, which either slow the process of cell death or inhibit cholinesterase, an enzyme believed to break down a key neurotransmitter involved in learning and memory development
  • Last month, the Pharmaceutical Research and Manufacturers of America, or PhRMA, reported that only three of 104 possible treatments have been approved in the past 13 years
  • Development of the WSU drug is only starting
  • Safety testing alone could cost more than $1 million
  • been working on their compound since 1992
  • practical utility of these early drug candidates, however, was severely limited
  • they were very quickly broken down by the body and couldn't get across the blood-brain barrier,
  • cellular barrier that prevents drugs and other molecules from entering the brain
  • 'That's useless. I mean, who wants to drill holes in people's heads?
  • designed a smaller version of the molecule
  • Not only is it stable but it can cross the blood-brain barrier
  • added bonus is it can move from the gut into the blood, so it can be taken in pill form
  • reported similar but less dramatic results in a smaller group of old rats. In this study the old rats
  • tested the drug on several dozen rats treated with scopolamine, a chemical that interferes with a neurotransmitter critical to learning and memory.
  • a rat treated with scopolamine will never learn the location of a submerged platform in a water tank, orienting with cues outside the tank
  • After receiving the WSU drug, however, all of the rats did, whether they received the drug directly in the brain, orally, or through an injection.
  • statistically valid, additional studies with larger test groups will be necessary to fully confirm the finding.
  • bench assays using living nerve cells to monitor new neuronal connections
  • Dihexa to be seven orders of magnitude more powerful than BDNF, which has yet to be effectively developed for therapeutic use
Mars Base

New drug could treat Alzheimer's, multiple sclerosis and brain injury - 0 views

medicalxpress.com/...-multiple-sclerosis-brain.html

Alzheimer MultipleSclerosis GrabBag

shared by Mars Base on 25 Jul 12 - No Cached
  • A new class of drug
  • shows early promise of being a one-size-fits-all therapy for Alzheimer's disease, Parkinson's disease, multiple sclerosis and traumatic brain injury by reducing inflammation in the brain
  • The drugs
  • ...22 more annotations...
  • target a particular type of brain inflammation
  • brain inflammation, also called neuroinflammation, is increasingly believed to play a major role in the progressive damage characteristic of these chronic diseases and brain injuries.
  • offers an entirely different therapeutic approach to Alzheimer's than current ones being tested to prevent the development of beta amyloid plaques in the brain
  • The plaques are an indicator of the disease but not a proven cause
  • given to a mouse genetically engineered to develop Alzheimer's, it prevents the development of the full-blown disease
  • identifies the optimal therapeutic time window for administering the drug, which is taken orally and easily crosses the blood-brain barrier.
  • In previous animal studies, the same drug reduced the neurological damage caused by closed-head traumatic brain injury and inhibited the development of a multiple sclerosis-like disease. In these diseases as well as in Alzheimer's, the studies show the therapy time window is critical
  • work by preventing the damaging overproduction of brain proteins called proinflammatory cytokines
  • Scientists now believe overproduction of these proteins contributes to the development of many degenerative neurological diseases
  • When too many of the cytokines are produced, the synapses of the brain begin to misfire
  • mouse model of Alzheimer's received MW151 three times a week starting at six months of age, right at the time the proinflammatory cytokines began to rise. This would be the comparable stage when a human patient would begin to experience mild cognitive impairment
  • drug protected against the damage associated with learning and memory impairment
  • before Alzheimer's memory changes are at a late stage may be a promising future approach to therapy
  • In M.S., overproduction of the proinflammatory cytokines damage the central nervous system and the brain
  • proteins directly or indirectly destroy the insulation or coverings of the nerve cells that transmit signals down the spinal cord
  • insulation is stripped, messages aren't properly conducted down the spinal cord
  • When mice that were induced to develop an M.S.-like disease received MW151 orally, they did not develop disease as severe.
  • After a traumatic brain injury, the glia cells in the brain become hyperactive and release a continuous cascade of proinflammatory cytokines
  • As a result of this hyperactivity, researchers believe the brain is more susceptible to serious damage following a second neurological injury.
  • when MW151 is given during an early therapeutic window three to six hours after the injury, it blocks glial activation and prevents the flood of proinflammatory cytokines after a traumatic brain injury
  • early on after traumatic brain injury or a even a stroke, you could possibly prevent the long-term complications of that injury including the risk of seizures, cognitive impairment and, perhaps, mental health issues
  • Stroke also causes inflammation in the brain that may also be linked to long-term complications including epilepsy and cognitive deficits
Mars Base

Alzheimer's: A Ray of Hope? Just Perhaps Maybe | Talking back, Scientific American Blog... - 0 views

blogs.scientificamerican.com/...ray-of-hope-just-perhaps-maybe

scibyte55 Alzheimer

shared by Mars Base on 19 Jul 12 - No Cached
  • pharmaceutical company Baxter International reported
  • a drug that, if it works in larger clinical trials now under way, might actually stabilize patients and stop disease progression
  • Gammagard, or intravenous immunoglobulin, a soup of antibodies extracted from blood donors and already approved for some immune disorders, halted for three years  any decline in cognition and in the ability to perform everyday tasks for four patients who received  the highest dose
  • ...13 more annotations...
  • Four patients
  • may be nothing
  • for sure
  • the drug may falter and go by the wayside as it makes its way through the clinical trials pipeline
  • results still intrigued some in the research community
  • Results from late-stage clinical trials next year will show whether these four were patients who just happened to have plateaued for a while during their inevitable decline
  • initial findings are encouraging, they are extremely preliminary
  • Until the results of the larger double-blind Phase 3 results demonstrate a significant benefit, intravenous immunoglobulin’s role in the treatment of AD is unproven
  • If later trials succeed, the results would give credence to the idea that Alzheimer’s usual suspect—a toxic peptide called amyloid-beta—is, in fact, the major heavy in the neurodegeneration
  • positive Phase III trial next year will mean, though, that the real work lies ahead
  • The drug, not covered by insurers, is already used off-label to treat Alzheimer’s by some rich patients who can afford to shell out $50,000 a year from their own pockets
  • If one day insurers were to cover Gammagard, not enough supply would exist for the donor-based drug—and shortages would make life difficult for  patients already using it for immune conditions
  • promising outcome for the drug trial may serve more as a proof of principle
Mars Base

Sub Glacial Lakes | Jupiter Broadcasting - 0 views

www.jupiterbroadcasting.com/...acial-lakes-updates-scibyte-33

scibyte42 Europa Alzheimer

shared by Mars Base on 12 Apr 12 - No Cached
Mars Base

Habitable Planets & Chimps | Jupiter Broadcasting - 0 views

www.jupiterbroadcasting.com/...able-planets-chimps-scibyte-24

scibyte42 Alzheimer

shared by Mars Base on 12 Apr 12 - No Cached
  • Habitable Planets & Chimps | SciByte 24
  • December 7, 2011
  • Alzheimer’s Research
1 - 20 of 24 Next ›
Showing 20▼ items per page