Archive for the ‘ALZHEIMERS’ Category

Compound reverses symptoms of Alzheimer’s and Parkinson’s in fruit flies

Wednesday, April 27th, 2016


The researchers tested the new method on fruit flies genetically altered to model the diseases.

Neurodegenerative disorders like Parkinson’s and Alzheimer’s are extremely widespread, affecting millions of people across the planet, but treatments are limited, and there’s currently no cure available. New work is showing promise in the development of a new treatment, with scientists identifying a compound that can reverse symptoms of the diseases. The method hasn’t been tested on human patients just yet, but it’s been found to be effective in genetically modified fruit flies.

Combating neurodegenerative disorders represents one of the biggest challenges in modern medicine. Our understanding of conditions like Alzheimer’s is improving rapidly, but actually finding effective treatments, and even cures, is proving extremely difficult.

The new study is a collaborative effort between the University of Maryland and the University of Leicester in the United Kingdom. It focuses on metabolites related to an amino acid called tryptophan, which breaks down into numerous compounds when it degrades in the body, which in turn have effects on the nervous system.

Two of these compounds are polar opposites, with 3-hydroxykynurenine (3-HK) having toxic properties and kynurenic acid (KYNA) helping to prevent nerve cell degeneration. The team believes that the amount of the two compounds present in the brain could play a big role in Alzheimer’s, Parkinson’s and Huntington’s disease.

To test that theory, they worked with fruits flies genetically altered to model Alzheimer’s and Parkinson’s diseases, giving them a chemical that inhibits an enzyme known as trytophan-2,3-dioxygenase (TDO). The enzyme controls the relationship between 3-HK and KYNA, with its inhibition shifting metabolism towards the latter. The effect on the flies was significant, improving their movement and lengthening their lifespans.

“A key finding of our study is that we can improve ‘symptoms’ in fruit fly models of Alzheimer’s and Parkinson’s disease by feeding them a drug-like chemical,” said study co-author Carlo Breda of the University of Leicester. “Our experiments have identified TDO as a very promising new drug target.”

Looking forward, the researchers hope to test the treatment on human patients to see if it does indeed represent a new means of combating neurodegenerative disorders.

The findings of the study are published online in the Proceedings of the National Academy of Sciences.

Source: University of Maryland


Henry Sapiecha

Brain sediment Protein discovery sheds light on Alzheimer’s disease

Sunday, April 17th, 2016

mitchondria – often referred to as the powerhouses of cells – play a role in the development of Alzheimer's.image

The new findings strongly suggest that mitchondria – often referred to as the powerhouses of cells – play a role in the development of Alzheimer’s.

Alzheimer’s disease is caused by a buildup of amyloid beta in the brain, which causes plaques that disrupt nerve cells. Now, research conducted by scientists at the University of Bergen is improving our understanding of exactly why this happens, identifying both a section of a cell and a protein that are central to the process.

Our understanding of Alzheimer’s disease is always evolving, with new discoveries being made every month. Just recently we’ve learned that mimicking movements could help patients relearn lost abilities, and we’ve even gained insights into how the disease impairs perception.

For the new research, the team studied patients with major physical and psychological problems, all of whom had a particular gene defect that causes a reduction in the amount of a particular protein in their systems, known as PITRM1.

Scanning the subjects’ brains revealed the telltale amyloid beta buildup in their brains. Further testing with laboratory mice exhibiting the same loss of PITRM1 backed up the finding, revealing a similar protein deposition in the brain.

Not only is the knowledge that the protein plays a central role in such neurological diseases likely to prove useful in developing new treatments, but the location of PITRM1 – found in mitochondria – confirms that these cell powerhouses play an important part as well.

“The results conclude a long discussion about the relationship between mitochondria and accumulation of amyloid in the brain” said research Janniche Torsvik. “We have found that mitochondria play a crucial role in the process of protein deposition.”

Full details of the research are published online in the journal EMBO Molecular Medicine.

Source: University of Bergen


Henry Sapiecha


Sunday, March 1st, 2015

Iron may be a factor in dementia

Dominic Hare at work in his laboratory. Photo: George Ganio

Alzheimer’s disease is no respecter of fame or fortune. Former US president Ronald Reagan had it. Legendary AC/DC guitarist Malcolm Young has been diagnosed. Hazel Hawke suffered until her death in 2013. And author and broadcaster Anne Deveson is experiencing the distressing progression of Alzheimer’s, the most common form of dementia, a group of brain disorders affecting thinking and memory.

There is no way to spot Alzheimer’s early, no effective treatment and no known cure. However, a neurochemist at the University of Technology, Sydney (UTS), Dr Dominic Hare, and his colleagues are homing in on a biomarker, or disease indicator, to help diagnosis.

Moreover, Dr Hare – who is also with the Florey Institute of Neuroscience and Mental Health in Melbourne and the Icahn School of Medicine at Mount Sinai in New York City – says the team’s work promises to help reveal the cause of the baffling disorder.

“The disease develops so slowly and has so many effects on the body, being able to separate what’s cause and what’s effect is a big problem,” he says. “If we can identify why the disease is happening, we could intervene to alleviate the symptoms and potentially halt the disease process.”

At present, a diagnosis of Alzheimer’s disease is made only after careful clinical consultation, and any diagnosis can be confirmed only by examining the brain after death.

However, Dr Hare and his co-workers are not looking in the brain for clues. They’re looking in the blood. In a recent article in the US journal ACS Neuroscience, the group outlined its work with a potential biomarker and a possible causative culprit: iron.

“The body uses metals like copper, zinc and iron to facilitate biochemical reactions it wants. In the case of disease, these are reactions that are unwanted,” Dr Hare says, adding that iron plays a very important role in the ageing process, and ageing is the key risk factor for Alzheimer’s disease. One in four people over the age of 85 have dementia; 75 per cent of those have Alzheimer’s.

Professor Perminder Sachdev, co-director of the Centre for Healthy Brain Ageing at the University of NSW, says metals have previously been linked to Alzheimer’s but the findings were inconclusive.

“This study by Dr Hare and his colleagues is, therefore, of interest to researchers in the field,” says Professor Sachdev, chief medical adviser to Alzheimer’s Australia.

Specifically, Dr Hare’s team is studying transferrin, a protein that helps ferry iron around the body.  In the case of Alzheimer’s, if transferrin falls down on the job iron may accumulate in the brain, where it contributes to the build-up of “plaques” and “tangles”. Plaques impede the transmission of signals among brain cells and tangles kill them.

To track transferrin’s activity, Dr Hare teamed up with Dr Blaine Roberts, head of the Metalloproteomics Laboratory at the Florey Institute. They designed the research using blood samples collected for the Australian Imaging, Biomarker & Lifestyle Flagship Study of Ageing (AIBL).

The multi-disciplinary, multi-institutional project is one of world’s largest studies of the biomarkers, cognitive characteristics and lifestyle factors implicated in Alzheimer’s.

“Putting all these pieces together will help find methods to maintain quality of life, possibly slowing or even halting the progress of the disease.”

Dr Dominic Hare

“The unique thing about AIBL is that it’s following 1000 people through time,” Dr Hare says. “That gives us statistical power.” Participants provide blood samples and are tracked over 54 months.

Dr Hare, Dr Roberts and their colleagues used samples from 34 AIBL participants and 36 healthy participants.  They employed specialised equipment to analyse samples: an inductively coupled plasma-mass spectrometer (ICP-MS), and a size exclusion chromatography-inductively coupled plasma-mass spectrometer (SEC-ICP-MS).

The results revealed, first, that compared to healthy volunteers, participants with Alzheimer’s had lower levels of iron in their plasma, a condition linked with anaemia of unknown cause.

Intriguingly, results from the ICP-MS and SEC-ICP-MS tests, showed healthy and Alzheimer’s participants had the same amount of transferrin in their blood but that the amount of iron carried by the transferrin was lower in Alzheimer’s samples. The implication: transferrin isn’t shuttling excess iron efficiently from the brain.

“The next step is to look at a copper-binding protein called ceruloplasmin that interacts with transferrin,” says Dr Hare. “Putting all these pieces together will help find methods to maintain quality of life, possibly slowing or even halting the progress of the disease.”


Henry Sapiecha

Experimental drug compound found to reverse effects of Alzheimer’s in mice

Thursday, August 14th, 2014

Researchers at Yale University have discovered a drug shown to reverse the brain deficits of Alzheimer’s in mice


While there has been progress made in the fight against Alzheimer’s, our understanding of the dispiriting disease remains somewhat limited, with a definitive cure yet to be found. The latest development comes at the hands of researchers from Yale’s School of Medicine, who have discovered a new drug compound shown to reverse the effects of Alzheimer’s in mice.

The team’s research centers on a protein in the brain called STtriatal-Enriched tyrosine Phosphatase (STEP). While STEP is essential to regulating learning and memory, high levels prevent the strengthening of synapses in the brain. This synaptic strengthening is necessary for people to convert short-term memories into long-term memories, therefore disruption of the process can lead to a range of neuropsychiatric disorders, including Alzheimer’s.

The scientists studied thousands of molecules in search of one that would inhibit the negative effects of STEP. They identified the compound TC-2153 and proceeded to examine its efficacy in curtailing the impacts of STEP, observing a reversal of deficits in a number of cognitive exercises, including the mouse’s ability to remember objects it had seen previously.

“A single dose of the drug results in improved cognitive function in mice,” says Dr Paul Lombroso, professor in the Yale Child Study Center and lead author of the study. “Animals treated with TC compound were indistinguishable from a control group in several cognitive tasks.”

The team is now investigating the effects of TC-2153 in rats and non-human primates with cognitive defects to determine whether the compound is effective at improving cognitive deficits in other animal models. If the testing proves successful, the team says it will bring them one step closer to human trials.

The research findings were published in the journal PLOS Biology.

Source: Yale University

Henry Sapiecha


Thursday, May 23rd, 2013

Alzheimer’s disease can now be cured in mice-Are humans next?

Although no one is announcing a cure for Alzheimer’s disease just yet, research recently conducted at the University of Southern California does at least offer a glimmer of hope. Using drugs known as TSPO (translocator protein) ligands, scientists there have successfully halted and even reversed the effects of Alzheimer’s in mice.


The mice, all of which were male, had been genetically engineered to develop the disease. The drugs were tested on both 7-month-old young adult mice and 24-month-old elderly mice. Because the TSPO ligands increase production of steroid hormones, it was important that the animals’ existing testosterone levels be kept low before beginning the treatment. While this had already occurred naturally with the older mice as a result of aging, the younger ones had to be castrated in order to bring their levels down.

After receiving once-a-week treatments for four weeks, all of the mice showed improvements. This was particularly noteworthy with the older mice, as their Alzheimer’s had become quite severe. After the four treatments, however, they showed “significant lowering of Alzheimer’s-related pathology and improvements in memory behavior.”

It’s already known that TSPO ligands help protect nerve cells by reducing inflammation, and that they increase the production of neuroactive hormones in the brain. The scientists now plan on determining which factor plays more of a part in the success with the mice, then developing new TSPO ligands designed around those findings.

“From the optimistic perspective, our data provide very promising findings with tangible potential benefits for both the prevention and treatment of Alzheimer’s,” said lead scientist Prof. Christian Pike. “On the pessimistic side, research scientists have developed many interventions that cured Alzheimer’s in mice but have failed to show significant benefits in humans. A critical direction we are currently pursuing is successfully translating these findings into humans.”

A paper on the research was recently published in The Journal of Neuroscience

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Henry Sapiecha

Alzheimers is most times mis-diagnosed as the doctor explains in this video

Sunday, December 23rd, 2012

Alzheimers is not dignosed well

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Sourced & published by Henry Sapiecha


Sunday, March 4th, 2012

Protiens effect on alzheimers patients condition

There have been many reports on numerous different approaches by scientists looking to tackle Alzheimer’s disease. While some, such as the anticancer drug bexarotene and a compound known as J147, show great promise, there is still no approved treatment to slow the disease’s progression. The latest promising candidate for a treatment comes from Canada’s Simon Fraser University (SFU), where a team has concluded that ensuring that sugar levels in a brain protein known as tau are maintained could slow or prevent the fatal disease.

Tau proteins are abundant in neurons of the central nervous system where they stabilize microtubules, which act like highways inside cells that allow intracellular transport. Earlier research has shown that defective tau proteins can lead to Alzheimer’s disease and that linkage of sugar molecules to proteins like tau is essential in cells.

Previous research has also shown a naturally occurring enzyme known as O-GlcNAcase robs tau of these essential sugar molecules, resulting in an Alzheimer brain having clumps of tau have almost none of this sugar attached to them. This clumping is an early sign of the disease and the number of clumps correlates with its severity.

Using a chemically-created inhibitor called Thiamet-G, SFU chemistry professor David Vocadlo and his colleagues have been able to stop O-GlcNAcase from depleting tau proteins of sugar molecules. The researchers found that mice given a daily dose of Thiamet-G in their drinking water had fewer clumps of tau and maintained healthier brains.

“A lot of effort is needed to tackle this disease and different approaches should be pursued to maximize the chance of successfully fighting it,” said Vocadlo. “In the short term, we need to develop better inhibitors of the enzyme and test them in mice. Once we have better inhibitors, they can be clinically tested.”

The team’s paper, “Increasing O-GlcNAc slows neurodegeneration and stabilizes tau against aggregation,” is published in the journal Nature Chemical Biology.

Source: Simon Fraser University

Sourced & published by Henry Sapiecha


Monday, January 16th, 2012


IT MAY sound like a strange brew, but green tea and red light could provide a novel treatment for Alzheimer’s disease. Together, the two can destroy the rogue “plaques” that crowd the brains of people with the disease. The light makes it easier for the green-tea extract to get to work on the plaques.

Andrei Sommer at the University of Ulm in Germany, and colleagues, have previously used red light with a wavelength of 670 nanometres to transport cancer drugs into cells. The laser light pushes water out of the cells and when the laser is switched off, the cells “suck in” water and any other molecules, including drugs, from their surroundings.

Now, Sommer’s team have found that the same technique can be used to destroy the beta-amyloid plaques in Alzheimer’s. These plaques consist of abnormally folded peptides, and are thought to disrupt communication between nerve cells, leading to loss of memory and other symptoms.

The team bathed brain cells containing beta-amyloid in epigallocatechin gallate (EGCG) – a green-tea extract known to have beta-amyloid inhibiting properties – at the same time as stimulating the cells with red light. Beta-amyloid in the cells reduced by around 60 per cent. Shining the laser light alone onto cells reduced beta-amyloid by around 20 per cent (Photomedicine and Laser Surgery, DOI: 10.1089/pho.2011.3073).

It can be difficult getting drugs into the brain, but animal experiments show that the green-tea extract can penetrate the so-called blood-brain barrier when given orally together with red light. The light, which can penetrate tissue and bone, stimulates cell mitochondria to kick-start a process that increases the barrier’s permeability, says Sommer.

There is no reason why other drugs that attack beta-amyloid could not be delivered to the brain in the same way, he adds.

“This important research could form the basis of a potential treatment for Alzheimer’s, with or without complementary drug treatment,” says Mario Trelles, medical director of the Vilafortuny Medical Institute in Cambrils, Spain.

“The technique described could help to regulate and even stop the appearance of this disease,” he adds.

Sourced & published by Henry Sapiecha


Monday, November 7th, 2011


A new study pinpoints the importance of certain soluble proteins, called cytokines, in Alzheimer’s disease. The study focuses on one of these cytokines, tumor necrosis factor-alpha(TNF), a very critical component of the brain’s immune system. Normally, TNF finely regulates the transmission of neural impulses within the brain. The authors hypothesized that elevated levels of TNF in Alzheimer’s disease interacy adversely with this regulation. To reduce elevated TNF, the authors gave patients an injection of an anti-TNF therapeutic called etanercept. Excess TNF-alpha has been documented in the cerebrospinal fluid of patients with Alzheimer’s.

The new study documents a dramatic and unprecedented therapeutic effect in an Alzheimer’s patient: improvement within minutes following delivery of perispinal etanercept, which is etanercept given by injection in the spine. Etanercept (trade name Enbrel) binds and inactivates excess TNF. Etanercept is FDA approved to treat a number of immune-mediated disorders and is used off label in the study.

The use of anti-TNF therapeutics as a new treatment choice for many diseases, such as rheumatoid arthritis and potentially even Alzheimer’s, was recently chosen as one of the top 10 health stories of 2007 by the Harvard Health Letter.

Similarly, the Neurotechnology Industry Organization has recently selected new treatment targets revealed by neuroimmunology (such as excess TNF) as one of the top 10 Neuroscience Trends of 2007. And the Dana Alliance for Brain Initiatives has chosen the pilot study using perispinal etanercept for Alzheimer’s for inclusion and discussion in their 2007 Progress Report on Brain Research.

The lead author of the study, Edward Tobinick M.D., is an assistant clinical professor of medicine at the University of California, Los Angeles and director of the Institute for Neurological Research, a private medical group in Los Angeles. Hyman Gross, M.D., clinical professor of neurology at the University of Southern California, was co-author.

This study is accompanied by an extensive commentary by Sue Griffin, Ph.D., director of research at the Donald W. Reynolds Institute on Aging at the University of Arkansas for Medical Sciences (UAMS) in Little Rock Arkansaw and at the Geriatric Research and Clinical Center at the VA Hospital in Little Rock, who along with Robert Mrak, M.D., chairman of pathology at University of Toledo Medical School, are editors-in-chief of the Medical Journal of Neuroinflammation.

Griffin and Mrak are pioneers in the field of neuroinflammation. Griffin published an extensive landmark study in 1989 describing the association of cytokine overexpression in the brain and Alzheimer’s disease. Her research helped pave the way for the findings of the present study. Griffin has recently been selected for membership in the Dana Alliance for Brain Initiatives, a nonprofit organization of more than 200 leading neuroscientists, including ten Nobel laureates.

“It is unprecedented that we can see cognitive and behavioral improvement in a patient with established dementia within minutes of therapeutic intervention,” said Griffin. “It is imperative that the medical and scientific communities immediately undertake to further investigate and characterize the physiologic mechanisms involved. This gives all of us in Alzheimer’s research a tremendous new clue about new avenues of research, which is so exciting and so needed in the field of Alzheimer’s. Even though this report predominantly discusses a single patient, it is of significant scientific interest because of the potential insight it may give into the processes involved in the brain dysfunction of Alzheimer’s.”

While the article discusses one patient, many other patients with mild to severe Alzheimer’s received the treatment and all have shown sustained and significently marked improvement.

The new study, entitled “Rapid cognitive improvement in Alzheimer’s disease following perispinal etanercept administration,” and the accompanying commentary, entitled “Perispinal etanercept: Potential as an Alzheimer’s therapeutic,” are available on the Web site of the Journal of Neuroinflammation (

Author Hyman Gross, M.D., has no competing interests. Author Edward Tobinick, M.D. owns stock in Amgen, the manufacturer of etanercept, and has multiple issued and pending patents assigned to TACT IP LLC that describe the parenteral and perispinal use of etanercept for the treatment of Alzheimer’s disease and other neurological disorders, including, but not limited to, U.S. patents 6015557, 6177077, 6419934, 6419944, 6537549, 6982089, 7214658 and Australian patent 758523.

Sourced & published by Henry Sapiecha


Sunday, March 27th, 2011

Pink power can save your brain

Algae pigment chases dementia marker

Big Pharma’s going to hate this — and that means I love it already: One of the tiniest and most humble creatures on the planet could hold the key to preventing Alzheimer’s disease.

It’s an algae called Haematococcus pluvialis, and it sits literally at the bottom of the food chain.

Because of its pink pigment, which comes from the antioxidant astaxanthin, anything that eats this algae also turns pink… as do the creatures that eat those creatures, and so on.

Think shrimp, salmon and flamingos.

But to explain how it works, I’m going to have to take you from the bottom of the food chain to the brink of cutting-edge science, where researchers have been investigating a compound called phospholipid hydroperoxides.

It’s called PLOOH for short, but don’t snicker at the name — this stuff is deadly serious: It builds up in the red blood cells of dementia patients.

Now, Japanese researchers say astaxanthin can actually flush all that extra PLOOH right out of your system (OK, you can snicker a little).

In a double-blind experiment, 30 healthy volunteers between the ages of 50 and 69 years old were given either a placebo or 6 or 12 mg of astaxanthin a day for 12 weeks.

While the placebo patients had no change in PLOOH, those given the astaxanthin saw their levels plunge by between 40 and 50 percent, with those who took the higher dose getting the biggest benefit, according to the study in BMJ.

Since dementia can take so many years before it manifests, it may be decades before anyone can say for certain whether astaxanthin will stop it.

But there’s no reason to wait — because by then, it might be too late for you. And besides, there’s enough research on its other benefits that I’ve already been calling this stuff “the alpha antioxidant.”

And with 500 times the antioxidant power of vitamin E, it’s easy to see why.

Studies have found that astaxanthin can protect everything from your heart to your eyes — and since it’s sat at the bottom of the food chain for millions of years, you might sat it’s been time-tested by Mother Nature herself.

You can’t beat that kind of lab work!

Age-Related Macular Degeneration: the leading cause of blindness in the aging population
· Alzheimer’s and Parkinson’s Diseases: two of the most important neurodegenerative diseases
· Cholesterol Disease: ameliorates the effects of LDL, the “bad” cholesterol
· Inflammatory, chronic viral and autoimmune diseases
· Dyspepsia
· Semen fertility improvement
· Muscle function
· Sunburn from UV light
· Normalization of cardiac rhythm
· Anti-hypertension agent
· Stress management
· Benign Prostatic Hyperplasia (BPH)
· Stroke: repairs damage caused by lack of oxygen.

A demand for natural ASTAXANTHIN is now emerging in the fast-growing, multi-billion dollar nutraceutical market; in particular, increasing evidence suggests that ASTAXANTHIN was shown to be a much more powerful antioxidant than vitamins C and E, or than other carotenoids such as beta-carotene, lycopene, lutein and zeaxanthin, among others.
The enhanced activity of ASTAXANTHIN may stem from its molecular structure. ASTAXANTHIN belongs to the xanthophyll group of carotenoids, or the oxygenated carotenoids (see other members of the group in Fig. 1). The hydroxyl and keto functional groups (see Fig. 1) present in the ending ionone ring of ASTAXANTHIN may be responsible for its uniquely powerful antioxidant activity and for its ability to span the membrane bilayers as a direct result of its more polar configuration relative to other carotenoids (3,1014). Carotenoids with polar end groups like ASTAXANTHIN span the lipid membrane bilayer with their end groups located near the hydrophobic-hydrophilic interface, where free-radical attack first occurs.