Posts tagged alzheimer's disease
Articles and news from the latest research reports.
In search for Alzheimer’s drug, a major STEP forward
Researchers at Yale School of Medicine have discovered a new drug compound that reverses the brain deficits of Alzheimer’s disease in an animal model. Their findings are published in the Aug. 5 issue of the journal PLoS Biology.
The compound, TC-2153, inhibits the negative effects of a protein called STtriatal-Enriched tyrosine Phosphatase (STEP), which is key to regulating learning and memory. These cognitive functions are impaired in Alzheimer’s.
"Decreasing STEP levels reversed the effects of Alzheimer’s disease in mice," said lead author Paul Lombroso, M.D., professor in the Yale Child Study Center and in the Departments of Neurobiology and Psychiatry at Yale School of Medicine.
Lombroso and co-authors studied thousands of small molecules, searching for those that would inhibit STEP activity. Once identified, those STEP-inhibiting compounds were tested in brain cells to examine how effectively they could halt the effects of STEP. They examined the most promising compound in a mouse model of Alzheimer’s disease, and found a reversal of deficits in several cognitive exercises that gauged the animals’ ability to remember previously seen objects.
High levels of STEP proteins keep synapses in the brain from strengthening. Synaptic strengthening is a process that is required for people to turn short-term memories into long-term memories. When STEP is elevated in the brain, it depletes receptors from synaptic sites, and inactivates other proteins that are necessary for proper cognitive function. This disruption can result in Alzheimer’s disease or a number of neuropsychiatric and neurodegenerative disorders, all marked by cognitive deficits.
"The small molecule inhibitor is the result of a five-year collaborative effort to search for STEP inhibitors," said Lombroso. "A single dose of the drug results in improved cognitive function in mice. Animals treated with TC compound were indistinguishable from a control group in several cognitive tasks."
The team is currently testing the TC compound in other animals with cognitive defects, including rats and non-human primates. “These studies will determine whether the compound can improve cognitive deficits in other animal models,” said Lombroso. “Successful results will bring us a step closer to testing a drug that improves cognition in humans.”
(Source: eurekalert.org)
(Image caption: An abnormal protein, left, is intercepted by the UW’s compound that can bind to the toxic protein and neutralize it, as shown at right. Image courtesy: University of Washington)
New protein structure could help treat Alzheimer’s, related diseases
There is no cure for Alzheimer’s disease and other forms of dementia, but the research community is one step closer to finding treatment.
University of Washington bioengineers have designed a peptide structure that can stop the harmful changes of the body’s normal proteins into a state that’s linked to widespread diseases such as Alzheimer’s, Parkinson’s, heart disease, Type 2 diabetes and Lou Gehrig’s disease. The synthetic molecule blocks these proteins as they shift from their normal state into an abnormally folded form by targeting a toxic intermediate phase.
The discovery of a protein blocker could lead to ways to diagnose and even treat a large swath of diseases that are hard to pin down and rarely have a cure.
“If you can truly catch and neutralize the toxic version of these proteins, then you hopefully never get any further damage in the body,” said senior author Valerie Daggett, a UW professor of bioengineering. “What’s critical with this and what has never been done before is that a single peptide sequence will work against the toxic versions of a number of different amyloid proteins and peptides, regardless of their amino acid sequence or the normal 3-D structures.”
The findings were published online this month in the journal eLife.
More than 40 illnesses known as amyloid diseases – Alzheimer’s, Parkinson’s and rheumatoid arthritis are a few – are linked to the buildup of proteins after they have transformed from their normally folded, biologically active forms to abnormally folded, grouped deposits called fibrils or plaques. This happens naturally as we age, to a certain extent – our bodies don’t break down proteins as quickly as they should, causing higher concentrations in some parts of the body.
Each amyloid disease has a unique, abnormally folded protein or peptide structure, but often such diseases are misdiagnosed because symptoms can be similar and pinpointing which protein is present usually isn’t done until after death, in an autopsy.
As a result, many dementias are broadly diagnosed as Alzheimer’s disease without definitive proof, and other diseases can go undiagnosed and untreated.
The molecular structure of an amyloid protein can be only slightly different from a normal protein and can transform to a toxic state fairly easily, which is why amyloid diseases are so prevalent. The researchers built a protein structure, called “alpha sheet,” that complements the toxic structure of amyloid proteins that they discovered in computer simulations. The alpha sheet effectively attacks the toxic middle state the protein goes through as it transitions from normal to abnormal.
The structures could be tailored even further to bind specifically with the proteins in certain diseases, which could be useful for specific therapies.
The researchers hope their designed compounds could be used as diagnostics for amyloid diseases and as drugs to treat the diseases or at least slow progression.
“For example, patients could have a broad first-pass test done to see if they have an amyloid disease and then drill down further to determine which proteins are present to identify the specific disease,” Daggett said.
Researchers discover that Klotho is neuroprotective against Alzheimer’s disease
Boston University School of Medicine researchers may have found a way to delay or even prevent Alzheimer’s disease (AD). They discovered that pre-treatment of neurons with the anti-aging protein Klotho can prevent neuron death in the presence of the toxic amyloid protein and glutamate. These findings currently appear in the Journal of Biological Chemistry.
Alzheimer’s disease is the most frequent age-related dementia affecting 5.4 million Americans including 13 percent of people age 65 and older and more than 40 percent of people over the age of 85. In AD the cognitive decline and dementia result from the death of nerve cells that are involved in learning and memory. The amyloid protein and the excess of the neurotransmitter, glutamate are partially responsible for the neuronal demise.
Nerve cells were grown in petri dishes and treated with or without Klotho for four hours. Amyloid or glutamate then were added to the dish for 24 hours. In the dishes where Klotho was added, a much higher percentage of neurons survived than in the dishes without Klotho.
"Finding a neuroprotective agent that will protect nerve cells from amyloid that accumulates as a function of age in the brain is novel and of major importance," explained corresponding author Carmela R. Abraham, PhD, professor of biochemistry and pharmacology at BUSM. "We now have evidence that if more Klotho is present in the brain, it will protect the neurons from the oxidative stress induced by amyloid and glutamate.
According to the researchers, Klotho is a large protein that cannot penetrate the blood brain barrier so it can’t be administered by mouth or injection. However in a separate study the researchers have identified small molecules that can enter the brain and increase the levels of Klotho. “We believe that increasing Klotho levels with such compounds would improve the outcome for Alzheimer’s patients, and if started early enough would prevent further deterioration. This potential treatment has implications for other neurodegenerative diseases such as Parkinson’s, Huntington’s, ALS and brain trauma, as well,” added Abraham.
(Source: eurekalert.org)
Experiences at every stage of life contribute to cognitive abilities in old age
Early life experiences, such as childhood socioeconomic status and literacy, may have greater influence on the risk of cognitive impairment late in life than such demographic characteristics as race and ethnicity, a large study by researchers with the UC Davis Alzheimer’s Disease Center and the University of Victoria, Canada, has found.
“Declining cognitive function in older adults is a major personal and public health concern,” said Bruce Reed professor of neurology and associate director of the UC Davis Alzheimer’s Disease Center.
“But not all people lose cognitive function, and understanding the remarkable variability in cognitive trajectories as people age is of critical importance for prevention, treatment and planning to promote successful cognitive aging and minimize problems associated with cognitive decline.”
The study, “Life Experiences and Demographic Influences on Cognitive Function in Older Adults,” is published online in Neuropsychology, a journal of the American Psychological Association. It is one of the first comprehensive examinations of the multiple influences of varied demographic factors early in life and their relationship to cognitive aging.
The research was conducted in a group of over 300 diverse men and women who spoke either English or Spanish. They were recruited from senior citizen social, recreational and residential centers, as well as churches and health-care settings. At the time of recruitment, all study participants were 60 or older, and had no major psychiatric illnesses or life threatening medical illnesses. Participants were Caucasian, African-American or Hispanic.
The extensive testing included multidisciplinary diagnostic evaluations through the UC Davis Alzheimer’s Disease Center in either English or Spanish, which permitted comparisons across a diverse cohort of participants.
Consistent with previous research, the study found that non-Latino Caucasians scored 20 to 25 percent higher on tests of semantic memory (general knowledge) and 13 to 15 percent higher on tests of executive functioning compared to the other ethnic groups. However, ethnic differences in executive functioning disappeared and differences in semantic memory were reduced by 20 to 30 percent when group differences in childhood socioeconomic status, adult literacy and extent of physical activity during adulthood were considered.
“This study is unusual in that it examines how many different life experiences affect cognitive decline in late life,” said Dan Mungas, professor of neurology and associate director of the UC Davis Alzheimer’s Disease Research Center.
“It shows that variables like ethnicity and years of education that influence cognitive test scores in a single evaluation are not associated with rate of cognitive decline, but that specific life experiences like level of reading attainment and intellectually stimulating activities are predictive of the rate of late-life cognitive decline. This suggests that intellectual stimulation throughout the life span can reduce cognitive decline in old age.”
Regardless of ethnicity, advanced age and apolipoprotein-E (APOE genotype) were associated with increased cognitive decline over an average of four years that participants were followed. APOE is the largest known genetic risk factor for late-onset Alzheimer’s. Less decline was experienced by persons who reported more engagement in recreational activities in late life and who maintained their levels of activity engagement from middle age to old age. Single-word reading — the ability to decode a word on sight, which often is considered an indication of quality of educational experience — was also associated with less cognitive decline, a finding that was true for both English and Spanish readers, irrespective of their race or ethnicity. These findings suggest that early life experiences affect late-life cognition indirectly, through literacy and late-life recreational pursuits, the authors said.
“These findings are important,” explained Paul Brewster, lead author of the study, a doctoral student at the University of Victoria, Canada, and a pre-doctoral psychology intern at the UC San Diego Department of Psychiatry, “because it challenges earlier research that suggests associations between race and ethnicity, particularly among Latinos, and an increased risk of late-life cognitive impairment and dementia.
”Our findings suggest that the influences of demographic factors on late-life cognition may be reflective of broader socioeconomic factors, such as educational opportunity and related differences in physical and mental activity across the life span.”
(Source: ucdmc.ucdavis.edu)
Study Links Enzyme to Alzheimer’s Disease
Unclogging the body’s protein disposal system may improve memory in patients with Alzheimer’s disease (AD), according to a study from scientists at Kyungpook National University in Korea published in The Journal of Experimental Medicine.
In AD, various biochemical functions of brain cells go awry, leading to progressive neuronal damage and eventual memory loss. One example is the cellular disposal system, called autophagy, which is disrupted in patients with AD, causing the accumulation of toxic protein plaques characteristic of the disease. Jae-sung Bae and colleagues had earlier noted that the brains of AD patients have elevated levels of an enzyme called acid sphingomyelinase (ASM), which breaks down cell membrane lipids prevalent in the myelin sheath that coats nerve endings. But whether increased ASM directly contributes to AD (and if so, how) was unclear.
The group now finds that these two defects are linked. In mice with AD-like disease, elevated ASM activity clogged up the autophagy machinery resulting in the accumulation of undigested cellular waste. Reducing levels of ASM restored autophagy, lessened brain pathology, and improved learning and memory in the mice. Provided these results hold true in humans, interfering with ASM activity might prove to be an effective way to slow—and possibly reverse—neurodegeneration in patients with AD.
Transplantation of healthy new brain cells reverses learning and memory loss in Alzheimer’s disease model
A new study from the Gladstone Institutes has revealed a way to alleviate the learning and memory deficits caused by apoE4, the most important genetic risk factor for Alzheimer’s disease, improving cognition to normal levels in aged mice.
In the study, which was conducted in collaboration with researchers at UC San Francisco and published today in the Journal of Neuroscience, scientists transplanted inhibitory neuron progenitors—early-stage brain cells that have the capacity to develop into mature inhibitory neurons—into two mouse models of Alzheimer’s disease, apoE4 or apoE4 with accumulation of amyloid beta, another major contributor to Alzheimer’s. The transplants helped to replenish the brain by replacing cells lost due to apoE4, regulating brain activity and improving learning and memory abilities.
“This is the first time transplantation of inhibitory neuron progenitors has been used in aged Alzheimer’s disease models,” said first author Leslie Tong, a graduate student at the Gladstone Institutes and UCSF. “Working with older animals can be challenging from a technical standpoint, and it was amazing to see that the cells not only survived but affected activity and behavior.”
The success of the treatment in older mice, which corresponded to late adulthood in humans, is particularly important, as this would be the age that would be targeted were this method ever to be used therapeutically in people.
“This is a very important proof of concept study,” said senior author Yadong Huang, MD, PhD, an associate investigator at Gladstone Institutes and associate professor of neurology and pathology at UCSF. “The fact that we see a functional integration of these cells into the hippocampal circuitry and a complete rescue of learning and memory deficits in an aged model of Alzheimer’s disease is very exciting.”
A balance of excitatory and inhibitory activity in the brain is essential for normal function. However, in the apoE4 model of Alzheimer’s disease—a genetic risk factor that is carried by approximately 25% of the population and is involved in 60-75% of all Alzheimer’s cases—this balance gets disrupted due to a decline in inhibitory regulator cells that are essential in maintaining normal brain activity. The hippocampus, an important memory center in the brain, is particularly affected by this loss of inhibitory neurons, resulting in an increase in network activation that is thought to contribute to the learning and memory deficits characteristic of Alzheimer’s disease. The accumulation of amyloid beta in the brain has also been linked to this imbalance between excitatory and inhibitory activity in the brain.
In the current study, the researchers hoped that by grafting inhibitory neuron progenitors into the hippocampus of aged apoE4 mice, they would be able to combat these effects, replacing the lost cells and restoring normal function to the area. Remarkably, these new inhibitory neurons survived in the hippocampus, enhancing inhibitory signaling and rescuing impairments in learning and memory.
In addition, when these inhibitory progenitor cells were transplanted into apoE4 mice with an accumulation of amyloid beta, prior deficits were alleviated. However, the new inhibitory neurons did not affect amyloid beta levels, suggesting that the cognitive enhancement did not occur as a result of amyloid clearance, and amyloid did not impair the integration of the transplant.
According to Dr. Huang, the potential implications for these findings extend beyond the current methods used. “Stem cell therapy in humans is still a long way off. However, this study tells us that if there is any way we can enhance inhibitory neuron function in the hippocampus, like through the development of small molecule compounds, it may be beneficial for Alzheimer disease patients.”
(Source: gladstoneinstitutes.org)
US Alzheimer’s Rate Seems to Be Dropping
The rate of Alzheimer’s disease and other dementias is falling in the United States and some other rich countries — good news about an epidemic that is still growing simply because more people are living to an old age, new studies show.
An American over age 60 today has a 44 percent lower chance of developing dementia than a similar-aged person did roughly 30 years ago, the longest study of these trends in the U.S. concluded.
Dementia rates also are down in Germany, a study there found.
"For an individual, the actual risk of dementia seems to have declined," probably due to more education and control of health factors such as cholesterol and blood pressure, said Dr. Kenneth Langa. He is a University of Michigan expert on aging who discussed the studies Tuesday at the Alzheimer’s Association International Conference in Copenhagen.
The opposite is occurring in some poor countries that have lagged on education and health, where dementia seems to be rising.
More than 5.4 million Americans and 35 million people worldwide have Alzheimer’s, the most common form of dementia. It has no cure and current drugs only temporarily ease symptoms.
A drop in rates is a silver lining in the so-called silver tsunami — the expected wave of age-related health problems from an older population. Alzheimer’s will remain a major public health issue, but countries where rates are dropping may be able to lower current projections for spending and needed services, experts said.
Recent studies from the Netherlands, Sweden and England have suggested a decline, and the new research extends this look to some other parts of the world.
(Image: Thinkstock)
Smell and eye tests show potential to detect Alzheimer’s early
A decreased ability to identify odors might indicate the development of cognitive impairment and Alzheimer’s disease, while examinations of the eye could indicate the build-up of beta-amyloid, a protein associated with Alzheimer’s, in the brain, according to the results of four research trials reported today at the Alzheimer’s Association International Conference® 2014 (AAIC® 2014) in Copenhagen.
In two of the studies, the decreased ability to identify odors was significantly associated with loss of brain cell function and progression to Alzheimer’s disease. In two other studies, the level of beta-amyloid detected in the eye (a) was significantly correlated with the burden of beta-amyloid in the brain and (b) allowed researchers to accurately identify the people with Alzheimer’s in the studies.
Beta-amyloid protein is the primary material found in the sticky brain “plaques” characteristic of Alzheimer’s disease. It is known to build up in the brain many years before typical Alzheimer’s symptoms of memory loss and other cognitive problems.
"In the face of the growing worldwide Alzheimer’s disease epidemic, there is a pressing need for simple, less invasive diagnostic tests that will identify the risk of Alzheimer’s much earlier in the disease process," said Heather Snyder, Ph.D., Alzheimer’s Association director of Medical and Scientific Operations. "This is especially true as Alzheimer’s researchers move treatment and prevention trials earlier in the course of the disease."
"More research is needed in the very promising area of Alzheimer’s biomarkers because early detection is essential for early intervention and prevention, when new treatments become available. For now, these four studies reported at AAIC point to possible methods of early detection in a research setting to choose study populations for clinical trials of Alzheimer’s treatments and preventions," Snyder said.
With the support of the Alzheimer’s Association and the Alzheimer’s community, the United States created its first National Plan to Address Alzheimer’s Disease in 2012. The plan includes the critical goal, which was adopted by the G8 at the Dementia Summit in 2013, of preventing and effectively treating Alzheimer’s by 2025. It is only through strong implementation and adequate funding of the plan, including an additional $200 million in fiscal year 2015 for Alzheimer’s research, that we’ll meet that goal. For more information and to get involved, visit http://www.alz.org.
Clinically, at this time it is only possible to detect Alzheimer’s late in its development, when significant brain damage has already occurred. Biological markers of Alzheimer’s disease may be able to detect it at an earlier stage. For example, using brain PET imaging in conjunction with a specialized chemical that binds to beta-amyloid protein, the buildup of the protein as plaques in the brain can be revealed years before symptoms appear. These scans can be expensive and are not available everywhere. Amyloid can also be detected in cerebrospinal fluid through a lumbar puncture where a needle is inserted between two bones (vertebrae) in your lower back to remove a sample of the fluid that surrounds your brain and spinal cord.
(Image: Getty Images)
Discovery of New Drug Targets for Memory Impairment in Alzheimer’s Disease
We are now a step closer to having a drug that can cure dementia and memory loss. Research team in Korea has discovered that reactive astrocytes, which have been commonly observed in Alzheimer’s patients, aberrantly and abundantly produce the chief inhibitory neurotransmitter GABA and release it through the Best1 channel. The released GABA strongly inhibits neighboring neurons to cause impairment in synaptic transmission, plasticity and memory. This discovery will open a new chapter in the development of new drugs for treating such diseases.
Alzheimer’s disease, which is the most common cause of dementia, is fatal and currently, there is no cure. In Alzheimer’s disease, brain cells are damaged and destroyed, leading to devastating memory loss. It is reported that 1 in 8 Americans aged 65 or over have Alzheimer’s disease. In 2011, 7,600 elderly people with dementia lost their way back home and became homeless in Korea. However, to date, there has been no clear understanding of the mechanisms underlying dementia in Alzheimer’s disease. So far, neuronal death is the only proposed mechanism available in scientific literature.
The research team discovered that reactive astrocytes in the brains of Alzheimer’s disease model mice produce the inhibitory transmitter GABA by the enzyme Monoamine oxidase B(MAO-B) and release GABA through the Bestrophin-1 channel to suppress normal information flow during synaptic transmission. Based on this discovery, the team was able to reduce the production and release of GABA by inhibiting MAO-B or Bestrophin-1, and successfully ameliorate impairments in neuronal firing, synaptic transmission and memory in Alzheimer’s disease model mice.
In the behavioral test, the team used the fact that mice tend to prefer dark places. If a mouse experiences an electric shock in a dark place, it will remember this event and avoid dark places from then on. However, a mouse with modeled Alzheimer’s disease cannot remember if such shock is related to dark places and keeps going back to dark places. The team demonstrated that treating these mice with a MAO-B inhibitor fully recovered the mice’s memory. The selegiline is currently used in Parkinson’s disease as an adjunct therapy and considered as a one of best promising medicine for MAO-B inhibitor. But it has been previously shown to be less effective in Alzheimer’s disease.
The team proved that selegiline is effective for a short time, but when it is used in long term, it loses its efficacy in Alzheimer’s disease model mice. When treated for 1 week, selegiline brought the neuronal firing to a normal level. But when it was treated for 2 and 4 weeks, neuronal firing came back to the levels of untreated mice. From these results, the team proposed that there is a pressing need for a new drug that has long lasting effects.
Dr. C. Justin Lee said, “From this study, we reveal the novel mechanism of how Alzheimer’s patients might lose their memory. We also propose new therapeutic targets, which include GABA production and release mechanisms in reactive astrocytes for treatment of Alzheimer’s disease. Furthermore, we provide a stepping stone for the development of MAO-B inhibitors with long lasting efficacy.”
Significant step towards blood test for Alzheimer’s
Scientists have identified a set of 10 proteins in the blood which can predict the onset of Alzheimer’s, marking a significant step towards developing a blood test for the disease. The study, led by King’s College London and UK proteomics company, Proteome Sciences plc,analysed over 1,000 individuals and is the largest of its kind to date.
There are currently no effective long-lasting drug treatments for Alzheimer’s, and it is believed that many new clinical trials fail because drugs are given too late in the disease process. A blood test could be used to identify patients in the early stages of memory loss for clinical trials to find drugs to halt the progression of the disease.
The study, published in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association, is the result of an international collaboration led by King’s College London and Proteome Sciences plc, funded by Alzheimer’s Research UK, the UK Medical Research Council, the National Institute for Health Research (NIHR) Maudsley Biomedical Research Centre and Proteome Sciences.
The researchers used data from three international studies. Blood samples from a total of 1,148 individuals (476 with Alzheimer’s disease; 220 with ‘Mild Cognitive Impairment’ (MCI) and 452 elderly controls without dementia) were analysed for 26 proteins previously shown to be associated with Alzheimer’s disease. A sub-group of 476 individuals across all three groups also had an MRI brain scan.
Researchers identified 16 of these 26 proteins to be strongly associated with brain shrinkage in either MCI or Alzheimer’s. They then ran a second series of tests to establish which of these proteins could predict the progression from MCI to Alzheimer’s. They identified a combination of 10 proteins capable of predicting whether individuals with MCI would develop Alzheimer’s disease within a year, with an accuracy of 87 percent.
Dr Abdul Hye, lead author of the study from the Institute of Psychiatry at King’s College London, said: “Memory problems are very common, but the challenge is identifying who is likely to develop dementia. There are thousands of proteins in the blood, and this study is the culmination of many years’ work identifying which ones are clinically relevant. We now have a set of 10 proteins that can predict whether someone with early symptoms of memory loss, or mild cognitive impairment, will develop Alzheimer’s disease within a year, with a high level of accuracy.”
Professor Simon Lovestone, senior author of the study from the University of Oxford, who led the work whilst at King’s, said: “Alzheimer’s begins to affect the brain many years before patients are diagnosed with the disease. Many of our drug trials fail because by the time patients are given the drugs, the brain has already been too severely affected. A simple blood test could help us identify patients at a much earlier stage to take part in new trials and hopefully develop treatments which could prevent the progression of the disease. The next step will be to validate our findings in further sample sets, to see if we can improve accuracy and reduce the risk of misdiagnosis, and to develop a reliable test suitable to be used by doctors.”
Dr Eric Karran, Director of Research at Alzheimer’s Research UK, the UK’s leading dementia research charity, said: “As the onset of Alzheimer’s is often slow and subtle, a blood test to identify those at high risk of the disease at an early stage would be of real value. Detecting the first signs of Alzheimer’s could improve clinical trials for new treatments and help those already concerned about their memory, but we’re not currently in a position to use such a test to screen the general population.
“With an ageing population, and age the biggest risk factor for Alzheimer’s, we are expecting rising numbers of people to be affected over the coming years. It’s important to develop new ways to intervene early in the disease to help people maintain their quality of life for as long as possible.”
Dr Ian Pike, co-author of the paper from Proteome Sciences, said: “By linking the best British academic and commercial research, this landmark study in Alzheimer’s disease is a major advance in the development of a simple blood test to identify the disease before clinical symptoms appear. This is the window that will offer the best chance of successful treatment. Equally important, a blood test will be considerably easier and less expensive than using brain imaging or cerebrospinal spinal fluid.
“We are in the process of selecting commercial partners to combine the protein biomarkers in a blood test for the global market, a key step forward to deliver effective and early treatment for this crippling disease.”
Alzheimer’s disease is the most common form of dementia. Globally, it is estimated that 135 million people will have dementia by 2050. In 2010, the annual global cost of dementia was estimated at$604 billion. MCI includes problems with day-to-day memory, language and attention,and can be an early sign of dementia, or a symptom of stress or anxiety. Approximately 10% of people diagnosed with MCI develop dementia within a year but apart from regular assessments to measure memory decline, there is currently no accurate way of predicting who will, or won’t, develop dementia.
Previous studies have also shown that PET brain scans and plasma in lumbar fluid can be used to predict the onset of dementia from MCI. However, PET imaging is highly expensive and lumbar punctures invasive.
(Source: kcl.ac.uk)