Number of People with Alzheimer’s Disease May Triple by 2050

The number of people with Alzheimer’s disease is expected to triple in the next 40 years, according to a new study by researchers from Rush University Medical Center published in the February 6, 2013, online issue of Neurology, the medical journal of the American Academy of Neurology.

“This increase is due to an aging baby boom generation. It will place a huge burden on society, disabling more people who develop the disease, challenging their caregivers, and straining medical and social safety nets,” said co-author, Jennifer Weuve, MPH, ScD, assistant professor of medicine, Rush Institute for Healthy Aging at Rush University Medical Center in Chicago. “Our study draws attention to an urgent need for more research, treatments and preventive strategies to reduce the impact of this epidemic.”

For the study, researchers analyzed information from 10,802 African-American and Caucasian people living in Chicago, ages 65 and older between 1993 and 2011. Participants were interviewed and assessed for dementia every three years. Age, race and level of education were factored into the research.

The data was combined with U.S. death rates, education and current and future population estimates from the U.S. Census Bureau.

The study found that the total number of people with Alzheimer’s dementia in 2050 is projected to be 13.8 million, up from 4.7 million in 2010. About 7 million of those with the disease would be age 85 or older in 2050.

“Our projections use sophisticated methods and the most up-to-date data, but they echo projections made years and decades ago. All of these projections anticipate a future with a dramatic increase in the number of people with Alzheimer’s and should compel us to prepare for it,” said Weuve.

Treatment to prevent Alzheimer’s disease moves a step closer

A new drug to prevent the early stages of Alzheimer’s disease could enter clinical trials in a few years’ time according to scientists.

Alzheimer’s is the most common type of dementia, which currently affects 820,000 people in the UK, with numbers expected to more than double by 2050. One in three people over 65 will die with dementia.

The disease begins when a protein called amyloid-β (Aβ) starts to clump together in senile plaques in the brain, damaging nerve cells and leading to memory loss and confusion.

Professor David Allsop and Dr Mark Taylor at Lancaster University have successfully created a new drug which can reduce the number of senile plaques by a third, as well as more than doubling the number of new nerve cells in a particular region of the brain associated with memory.  It also markedly reduced the amount of brain inflammation and oxidative damage associated with the disease.

The drug was tested on transgenic mice containing two mutant human genes linked to inherited forms of Alzheimer’s, so that they would develop some of the changes associated with the illness. The drug is designed to cross the blood-brain barrier and prevent the Aβ molecules from sticking together to form plaques.

Professor Allsop, who led the research and was the first scientist to isolate senile plaques from human brain, said: “When we got the test results back, we were highly encouraged. The amount of plaque in the brain had been reduced by a third and this could be improved if we gave a larger dose of the drug, because at this stage, we don’t know what the optimal dose is.”

The drug needs to be tested for safety before it can enter human trials, but, if it passes this hurdle, the aim would be to give the drug to people with mild symptoms of memory loss before they develop the illness.

“Many people who are mildly forgetful may go on to develop the disease because these senile plaques start forming years before any symptoms manifest themselves. The ultimate aim is to give the drug at that stage to stop any more damage to the brain, before it’s too late.”

Support for the research was given by Alzheimer’s Research UK, and the results are published in the open access journal PLOS ONE.

First Alzheimer’s case has full diagnosis 106 years later

More than a hundred years after Alois Alzheimer identified Alzheimer’s disease in a patient an analysis of that original patient’s brain has revealed the genetic origin of their condition.

The brain specimen tested was discovered in a university basement late last century after a search by rival teams of academics.

"It is extremely satisfying to place this last piece in the medical puzzle that Auguste Deter, the first ever Alzheimer patient, presented us with,” said Professor Manuel Graeber, from the University of Sydney.

"It is not only of historical interest, however, as it ends any speculation about whether the disease is correctly named after Alois Alzheimer. Alzheimer’s ability to recognise this dementia more than a century ago provides compelling support for specialisation in medicine. Alzheimer was a founding father of neuropathology, an important medical specialty that is still underrepresented."

Professor Graeber, from the University’s Brain and Mind Research Institute, Sydney Medical School and the Faculty of Health Sciences, collaborated with Professor Ulrich Müller’s team from the Institute of Human Genetics of the University of Giessen in Germany to produce the molecular diagnosis recently published in Lancet Neurology.

For years scientists have been wondering whether the first case of Alzheimer’s disease had a genetic cause. In 1901 Auguste Deter, a middle-aged female patient at the Frankfurt Asylum with unusual symptoms, including short-term memory loss, came to the attention of Dr Alzheimer. When she died, Dr Alzheimer examined her brain and described the distinctive damage indicating a form of presenile dementia.

For decades the more than 200 slides that Alzheimer prepared from Deter’s brain were lost. Then in 1992, after Professor Graeber uncovered new information pointing to their location, two teams of medical researchers began a dramatic race to find them.

One team searched in Frankfurt but it was a team headed by Professor Graeber, then working at the Max Planck Institute for Neurobiology that finally located the material at the University of Munich in 1997.

The slides were examined and confirmed beyond doubt that Deter was suffering from Alzheimer’s disease, with large numbers of amyloid plaques and neurofribrillary tangles in the brain that are hallmarks of the disease. Until now a more sophisticated DNA analysis of the small amount of fragile material in single slides has not been possible.

Since their rediscovery, a significant number of brain slides have been under the official custodianship of Professor Graeber who has been at the University of Sydney since 2010. He is preparing a book on the material.

"We found a mutation whose ultimate effect is the formation of amyloid plaques. These plaques, which form between nerve cells and seem to suffocate them are the key diagnostic landmark of the disease."

Alzheimer’s disease represents one of the greatest health problems in industrialised societies today. An estimated 100 million dementia sufferers are predicted worldwide by 2050, the vast majority of whom will have Alzheimer’s disease.

95 percent of Alzheimer’s patients suffer late onset of the illness after they turn 65. Five percent fall ill before that age (early onset) and Auguste Deter belongs to this group.

"We have revealed that Auguste Deter is one of those in which early onset of the disease is caused by mutation in a single gene," said Professor Graeber.

Can Blood Pressure Drugs Reduce the Risk of Dementia?

People taking the blood pressure drugs called beta blockers may be less likely to have changes in the brain that can be signs of Alzheimer’s disease and other types of dementia, according to a study released today that will be presented at the American Academy of Neurology’s 65th Annual Meeting in San Diego, March 16 to 23, 2013. The study involved 774 elderly Japanese-American men who took part in the Honolulu-Asia Aging Study. Autopsies were performed on the men after their death. Of the 774 men, 610 had high blood pressure or were being treated with medication for high blood pressure. Among those who had been treated (about 350), 15 percent received only a beta blocker medication, 18 percent received a beta blocker plus one or more other medications, and the rest of the participants received other blood pressure drugs.

The study found that all types of blood pressure treatments were clearly better than no treatment. However, men who had received beta blockers as their only blood pressure medication had fewer abnormalities in their brains compared to those who had not been treated for their hypertension, or who had received other blood pressure medications. The brains of participants who had received beta blockers plus other medications showed an intermediate reduction in numbers of brain abnormalities.

These included two distinct types of brain lesion: those indicating Alzheimer’s disease, and lesions called microinfarcts, usually attributed to tiny, multiple, unrecognized strokes. Study participants who had taken beta blockers alone or in combination with another blood pressure medication had significantly less shrinkage in their brains.

“With the number of people with Alzheimer’s disease expected to grow significantly as our population ages, it is increasingly important to identify factors that could delay or prevent the disease,” said study author Lon White, MD, of the Pacific Health Research and Education Institute in Honolulu. “These results are exciting, especially since beta blockers are a common treatment for high blood pressure.”

Earlier research has shown that high blood pressure in midlife is a strong risk factor for dementia.

PredictAD software promises early diagnosis of Alzheimer’s

Scientists at VTT Technical Research Centre in Finland have developed new software called PredictAD that could significantly boost the early diagnosis of Alzheimer’s disease.

The comparative software contrasts patient’s measurements with those of other patients kept in large databases, then visualizes the status of the patient with an index and graphics.

The support system and imaging methods were developed by VTT and Imperial College London.

The researchers used material compiled in the U.S. by the Alzheimer’s Disease Neuroimaging Initiative based on the records of 288 patients with memory problems. Nearly half of them, or 140 individuals, were diagnosed with Alzheimer’s disease on average 21 months after the initial measurements, which is about the same as the current European average of 20 months.

The researchers concluded that half of the patients could have been diagnosed with the disease around a year earlier, or nine months after the initial measurements. They say the accuracy of the predictions was comparable to clinical diagnosis.

There are several advantages of an early diagnosis of Alzheimer’s. It can delay institutionalization and slow down the progress of the disease. It is also advantageous from the clinical trials perspective because if patients caught early can be included in the trials, treatment is likely to be more effective.

Working towards the same goal, researchers at Lancaster University in the U.K. recently developed an eye test method to detect early signs of Alzheimer’s.

The VTT researchers will spend the next five years carrying out the test at memory clinics in Europe. They also hope to expand its scope to include other illnesses that cause dementia. According to 2010 figures, an estimated 35.6 people live with dementia worldwide, and that number is expected to rise to 65.7 million by 2030.

The findings of the research were published in the Journal of Alzheimer’s Disease in November 2012. VTT cooperated with the University of Eastern Finland and Copenhagen University Hospital Rigshospitalet on this project.

Study Details Brain Damage Triggered by Mini-Strokes

A new study appearing today in the Journal of Neuroscience details for the first time how “mini-strokes” cause prolonged periods of brain damage and result in cognitive impairment. These strokes, which are often imperceptible, are common in older adults and are believed to contribute to dementia. 

“Our research indicates that neurons are being lost as a result of delayed processes following a mini-strokes that may differ fundamentally from those of acute ischemic events,” said Maiken Nedergaard, M.D., D.M.Sc., the lead author of the study and professor of Neurosurgery at the University of Rochester Medical Center (URMC). “This observation suggests that the therapeutic window to protect cells after these tiny strokes may extend to days and weeks after the initial injury.”

The prevalence of mini-strokes, or microinfarcts, has only been recently appreciated because common imaging techniques, such as MRI, are typically not sensitive enough to detect these microscopic injuries.

Similar to severe ischemic strokes, mini-strokes are caused when blood flow is blocked to a small area of the brain, usually by particle that travelled there from another part of the body. But unlike acute ischemic strokes – which bring about immediate symptoms such as numbness, blurry vision, and slurred speech – mini-strokes usually pass without notice. However, it is increasingly appreciated that these smaller strokes have a lasting impact on neurological function.

Microinfarcts are far more common than previously understood; it is believed that about 50 percent of individuals over the age of 60 have experienced at least one mini-stroke. Studies have also correlated the presence of mini-strokes with the symptoms of dementia. An estimated 55 percent of individuals with mild dementia and upwards of 70 percent of individuals with more severe symptoms show evidence of past mini-strokes. This association has led researchers to believe that these mini-strokes may be key contributors to age-related cognitive decline and dementia.

Nedergaard and her colleagues were the first to develop an animal model in which the complex progression and, ultimately, the cognitive impact of mini-strokes could be observed. Her team found that, in most instances, these strokes result in a prolonged period of damage to the brain.

Mayo Clinic Researchers Uncover Toxic Interaction in Neurons that Leads to Dementia and ALS

Researchers at Mayo Clinic in Florida have uncovered a toxic cellular process by which a protein that maintains the health of neurons becomes deficient and can lead to dementia. The findings shed new light on the link between culprits implicated in two devastating neurological diseases: frontotemporal dementia and amyotrophic lateral sclerosis, also known as Lou Gehrig’s disease. The study is published Dec. 10 in the online issue of Proceedings of the National Academy of Sciences.

There is no cure for frontotemporal dementia, a disorder that affects personality, behavior and language and is second only to Alzheimer’s disease as the most common form of early-onset dementia. While much research is devoted to understanding the role of each defective protein in these diseases, the team at Mayo Clinic took a new approach to examine the interplay between TDP-43, a protein that regulates messenger ribonucleic acid (mRNA) — biological molecules that carry the information of genes and are used by cells to guide protein synthesis — and sortilin, which regulates the protein progranulin.

"We sought to investigate how TDP-43 regulates the levels of the protein progranulin, given that extreme progranulin levels at either end of the spectrum, too low or too high, can respectively lead to neurodegeneration or cancer," says the study’s lead investigator, Mercedes Prudencio, Ph.D., a neuroscientist at the Mayo Clinic campus in Florida.

The neuroscientists found that a lack of the protein TDP-43, long implicated in frontotemporal dementia and amyotrophic lateral sclerosis, leads to elevated levels of defective sortilin mRNA. The research team is the first to identify significantly elevated levels of the defective sortilin mRNA in autopsied human brain tissue of frontotemporal dementia/TDP cases, the most common subtype of the disease.