Alarming new study: Alzheimer’s disease may spread through blood transfusions

Can you catch Alzheimer’s? Can Alzheimer’s disease spread through blood transfusion? These questions have been asked by many, but there were no positive proof. But now, a new study suggests the disease might spread through blood transfusion.

Researchers from the University of British Columbia have found that healthy mouse who shared blood with another mouse who had Alzheimer's plaques did actually develop beta-amyloid plaques in its brain.

However, Professor Weihong Song, the lead researcher of the study said, people shouldn’t be frightened about catching Alzheimer’s disease through blood transfusions.

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He said that in humans, beta-amyloid protein may pass through blood transfusions whether they have Alzheimer’s or not, because the protein can be manufactured outside the brain.

However, the chances of a healthy person developing beta-amyloid plaques in the brain via blood transfusion are very little because very low level of beta-amyloid can be exchanged. 

Beta-amyloid plaques are one of the hallmarks of Alzheimer’s disease. They are found between neurons in the brain. Beta-amyloid is a protein bit clipped from an APP (amyloid precursor protein). Inside the brain of a healthy person, these protein fragments get broken down and removed. However, in Alzheimer's patients, these sticky fragments gather to form solid, insoluble senile plaques.

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Beta-amyloid protein starts to kill synapses – connections between neurons. After destroying synapses the protein clumps into senile plaque, which destroys the nerve cells.

The death of nerve cells cause the Alzheimer’s patient to gradually loose memory, learning and the person eventually becomes unfit to perform simple everyday tasks like tying shoelaces.

Alzheimer's cells showing beta-amyloid plaques

For their study, the team inserted beta-amyloid gene into healthy mice, which enabled the rodents to develop beta-amyloid plaques similar to the type seen in human Alzheimer’s patients.

The researchers then surgically attached each beta-amyloid gene carrying mouse to a mouse without the gene. The process simulated a shared blood system.

The healthy mice started to amass beta-amyloid in their brains, and after remaining attached for a year, the healthy mice developed Alzheimer’s. In the areas of the brain that were crucial for learning and memory, the infected mice showed destructive activities observed in Alzheimer’s.

Prof. Song said the protein can enter the brain from an attached mouse with beta-amyloid and cause neurodegeneration. [মধুর যত মধুর গুণাবলী]

A different study conducted last year, showed approximately 1.4 million who received blood transfusions from people with Parkinson’s disease and other forms of dementia in the UK, weren’t likely to get the diseases.

Professor Tara Spires-Jones of the University of Edinburgh, in the UK, said this is vital for us to understand the biological changes in our body and how toxic proteins spread, but this is very distant from Alzheimer’s disease in humans.

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Slow walking speed may be a sign of Alzheimer’s onset, say scientists

The phrase “Slow and steady wins the race” may not apply to all seniors. According to a research published in the journal Neurology, speed of walking in elderly people may indicate their probability of developing Alzheimer’s disease.

Slow walking is very common in elderly, but a research from France indicates it may be a sign of Alzheimer’s onset.

According to Dr. Laura Phipps of the Alzheimer’s Research UK, while Alzheimer’s disease is associated with forgetfulness and confusion, there may be other physical symptoms like mobility problems which may indicate Alzheimer’s.

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The research team led by Natalia del Campo, PhD, of the Gerontopole and the Center of Excellence in Neurodegeneration of Toulouse, in France, concluded that a slower pace of walking may be associated with the amount of beta amyloid Alzheimer’s patients have accumulated in their brains, even if the external symptoms of Alzheimer’s aren’t yet present in them.

The accumulated clumps of beta-amyloid are known as amyloid plaques. Amyloid plaques are considered one of the hallmarks of Alzheimer’s disease. Scientists believe build-up of amyloid plaques in and around hippocampus are responsible for the death of brain cells, which triggers the disease.

Alzheimer’s is the most common cause of dementia, accounting for about 60-70% of all dementia cases. The most common early symptom is short-term memory loss.

Alzheimer’s has been recently ranked as the sixth leading cause of death in the United States. An estimated 5.3 million Americans of all ages have Alzheimer’s.

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Around 800,000 people in UK are affected by the disease.

Age is one of the risk factors of Alzheimer’s. People over the age of 70 are at a higher risk of developing Alzheimer’s.

PET (Positron Emission Tomography) scans were performed on the participants' brains 

The team studied 128 seniors whose average age was 76 years, and were deemed at high risk of developing dementia because of their memory problems.

PET (Positron Emission Tomography) scans on their brains showed that 48% of them had amyloid levels often linked with dementia. Their cognitive skills and their ability to complete day-to-day activities were also tested.

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Of the participants, 46% had mild cognitive decline, which may indicate the start of dementia that arises in Alzheimer’s.

The participants’ walking speed was measured using a standard test that measures the time of how fast they walk approximately 13 feet at their own speed. The average walking speed of the seniors was 3.48 feet/second (2.3 miles/hour). All except 2 of the participants had normal walking speed.

The researcher discovered that amyloid levels accounted for up to 9 percent of the differentiation in the speed of walking. They found a connection between slow walking and amyloid in several parts of the brain, including putamen, a crucial area of the brain involved in motor function. The seniors who walked more slowly had greater accumulation of the protein amyloid. [এই ৭টি খাবার আপনাকে ওজন কমাতে সাহায্য করবে ]

There was no changes in connections between levels of amyloid and speed of walking, when their age, level of education or level of memory problems were taken into account.

Dr. del Campo says that it is possible that experiencing subtle walking disturbances along with memory concerns may indicate Alzheimer’s disease, even before any clinical symptoms are displayed. [Read more 7 Foods That Will Help You Lose Weight]

Del Campo notes, however, that the study only shows a link between amyloid and speed of walking but it does not prove that amyloid accumulation is the cause of slow walking. There are many factors that cause older people to walk slowly.

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Hearing loss tied to Alzheimer’s disease

As we get older, certain sounds become more difficult to hear. But, doctors say untreated hearing loss could put patients in risk for serious health problems.

“You can lose and additional cubic sonometer of brain tissue a year, if you have untreated hearing loss. That’s why it’s so important to test for it,” says neurologist Dr. Fredrick Shaerf in an interview with Lee Health.

According to experts, advanced hearing loss puts patients at risk for developing Alzheimer’s disease.

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Alzheimer's disease is a neurodegenerative disease that normally starts slowly and deteriorates over time. It is the most common cause of dementia, accounting for about 60-70% of all cases. While it starts out with short-term memory loss, the disease progresses rapidly, rendering the inflicted person unable to perform simple every tasks such as using the phone or tying shoelaces.

  

“There is significant risk of developing a dementia if they have untreated hearing loss; and those risks can be up to five times the risk if you have severe hearing loss, three times moderate, twice mild. So, that’s a significant risk with something that’s treatable,” Dr. Shaerf says.

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In 2016, the Better Hearing Institute highlighted the importance of hearing health to general cognitive function, due to a growing body of study linking untreated hearing loss to memory loss and decreased cognitive function.

Arthur Wingfield, PhD, Professor of Neuroscience at the Brandeis University, has been studying intellectual aging and the association between memory and hearing keenness for several years. He says that untreated hearing loss makes the person to put more effort while listening, which can lead to elevated stress and poorer results in memory tests.

Dr. Shaerf says that we don’t realize we have a hearing loss.

Hearing loss can be treated with things like hearing aids. About one-third of people who are 65 years or old, have hearing loss, but about 15 percent wear hearing aids.

“Well, it seems to be a risk because the information is not getting in. And therefore, in the speech and language centers, it’s not sort of not getting the stimulation, and we know when nerves don’t get stimulated, they shrink or atrophy,” Dr. Shaerf says.

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He recommends that patients have their hearing and cognition tests regularly.

“We also know that we don’t realize we have a hearing loss. And most of us who develop it lose some of the high-pitched tones so we hear the television when it’s up loud enough; we don’t think that there’s a problem, when there really is,” says Dr. Shaerf.

Recognizing and treating hearing loss early can prevent hearing loss problems, including the development of Alzheimer’s disease.

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Brain electrodes may help Alzheimer’s patients keep memories

Brain electrodes developed by researchers from the University of South Carolina and North Carolina’s Wake Forest Baptist Medical Center may help people suffering from memory loss and soldiers with brain-damage recapture their memories.

An estimated 5.5 million Americans have Alzheimer’s disease, according to a 2015 report. It is the sixth leading cause of death in the US. 1 in 3 seniors in the US die with Alzheimer’s or some other form of dementia. Alzheimer’s affects almost 800,000 people in the UK.

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In a normal brain, when sensory inputs in the forms of sights, sounds, smells, and feelings are sent, it creates a memory by sending complex electrical signals through the hippocampus region. 

Hippocampus is the part of the brain where memories are stored. The signals are then encoded at each region until it reaches the final region, where a completely different signal is sent for long-term storage.

However, if there is damage in any of the regions, it prevents the encoding and the brain fails to form a long-term memory. This is why Alzheimer’s patients can recall events that happened in the past before the brain damage, but cannot form new long-term memories due to hippocampus damage.

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For the implant, electrodes are placed in hippocampus region of the brain. It has shown promising results in tests on rats and monkeys. Then they successfully used it on humans.

Researchers used patients with chronic seizures who had brain electrodes implanted in the hippocampus region of the brain for their treatment.

The brain electrodes were used on hundreds of trial that involved 9 patients, the algorithm accurately predicted how the signals would be translated about 90% of the time.

Ted Berger, a scientist from the Wake Forest involved with this project explains it like being capable of translating from Spanish to French without knowing either language.

This test suggests that a device can be designed to replace or support functions in the part of the brain that is damaged, said Robert Hampson of Wake Forest Baptist.

Researchers hope that this project with brain electrodes will help treat neurodegenerative disease like Alzheimer’s disease.

Brain electrodes are also being tested on paraplegics to help them perform simple movements with robotic arms or their limbs.

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Dr. Clare Walton, research manager at UK’s Alzheimer’s Society believes this device, if successfully tested in humans, could be an effective treatment for specific dementia symptoms, but it will not slow the progression of the disease or cure it.

Now, the researchers using brain electrodes are attempting to send back the translated signal in the brains of Alzheimer’s patients to try to bypass the damaged region, thereby allowing the formation of long-term memories.

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Anxiety may be an early indicator of Alzheimer's disease in older adults

A new study suggests anxiety may be an early warning sign of Alzheimer’s disease. The results support the theory that neuropsychiatric symptoms could depict the early signs of Alzheimer’s.

Researchers found that heightening symptoms of anxiety were associated with greater levels of beta-amyloid in the brains of elderly without impaired cognition. Beta-amyloid is a protein linked with Alzheimer's, and is one of the hallmarks of the disease.

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Scientists have long investigated risk factors, such as depression, that could result in Alzheimer’s. But this new study took a more distinct approach and examined the symptoms of depression – such as anxiety – itself.

Anxiety disorders, which affect almost 40 million adults each year, are common throughout the United States.

Alzheimer’s is a progressive neurodegenerative disease that causes cognitive decline and eventually renders the inflicted person incapable of carrying out simple tasks such as buttoning a shirt or using the phone. Approximately 5.5 million adults in the United States are affected by the disease, among them 5.4 million are older than 65 years.

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For their study, Dr. Nancy Donovan, from Brigham and Women's Hospital, and colleagues analyzed data of 270 healthy adults, who were part of the Harvard Aging Brain Study, for five years. The adults were aged between 62 and 90.

All the participants underwent positron emission tomography (PET) scan at the study onset and yearly during the 5-year follow-up period.

Researchers used 30-item Geriatric Depression Scale (GDS) to assess depression symptoms among these adults. They also evaluated scores for 3 conglomerations of depression symptoms: anxiety, apathy-anhedonia, and dysphoria.

Higher levels of beta-amyloid in the brain was linked with increasing symptoms of anxiety in older adults who didn’t have cognitive impairment.

The researchers found that higher levels of beta-amyloid in the brain was linked with increasing symptoms of anxiety in older adults who didn’t have cognitive impairment.

The findings suggest that increasing symptoms of anxious-depression may be an early sign of elevated levels of beta-amyloid, and in turn Alzheimer’s disease.

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The team says the results back the hypothesis that appearing neuropsychiatric symptoms constitute an early indication of preclinical Alzheimer’s.

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Dr. Donovan and her team concluded that a bigger study focusing on the same subject is required to further confirm these initial findings. However, the anxiety testing could be a practical tool to ascertain if a person is at heightened risk of developing Alzheimer’s disease, they added.

The findings were printed in The American Journal of Psychiatry.

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Urine test for early Alzheimer’s may be on the horizon

A joint study by Philadelphia’s Monell Chemical Sense Center and the U.S. Department of Agriculture (USDA) suggests the possibility of detecting early stages of Alzheimer’s disease from the odor signature of urine. Although the study was done on mice and a lot of work needs to be done, researchers are hopeful the findings will lead to a non-invasive urine test that diagnoses the neurodegenerative disease before it finds time to do too much damage to the brain.

Dr. Bruce Kimball, an author of the study, and a chemical ecologist with the USDA NWRC, said before this study they focused mostly on alterations in body smell caused by elements that derive outside the body, for example viruses and vaccines.

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Dr. Kimball said the findings may be useful for other neurologic diseases as well, since they now know that odor signatures of the urine can be changed by alterations in the brain typical of Alzheimer’s.

Alzheimer's is a progressive neurodegenerative disease that slowly destroys memory and cognitive skills, and eventually the ability to carry out simplest tasks. It is the most common form of dementia, accounting for about 60-70% of all dementia cases.

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Alzheimer’s has been recently ranked as the third leading cause of death in the United States. An estimated 5.3 million Americans have Alzheimer’s.

Around 800,000 people in the UK are affected by Alzheimer’s disease.

Although, the exact cause of the disease is not known, AlFuois Alzheimer, the German psychiatrist who described the disease, identified two hallmarks of the disease – abnormal quantities of protein (amyloid plaques) and fibers (tau tangles) in the brain.

While there is no way to reverse or stop the progression of this dreaded disease yet, an early and accurate diagnosis would provide patients and their caregivers time to plan and the healthcare professionals time to discover a treatment to ease the symptoms.

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For their study, the researchers worked with mice that artificially developed amyloid plaques in their brains same as the ones found in the brains of Alzheimer’s patients. For the breeding process, scientists inserted human genes into the genomes of the mice then used drugs to activate them. The mutations in the genes cause the brain cells of the mice to produce excessive amyloid precursor protein.

These types of mice are known as APP (amyloid precursor protein transgenic) mice. These mice similar behavioral symptoms of mental deterioration.

In the modified mice brain, the amyloid plaques clog the brain in a similar way that is observed in humans with Alzheimer’s disease.

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The researchers used three different strains of APP mice. After using behavioral and chemical analysis, the team discovered that each strain of these APP mice had specific urine smell signatures that were noticeably different from those mice in the control group.

The odor changes were not the result of new compounds being created in the body, but instead were changes in concentrations of normal urinary compounds.

The odor differences between control mice and those with Alzheimer's predated detectable quantities of plaque accumulation in the APP mice brains. Further studies revealed that the definite odor profiles could be used to pinpoint APP mice against control mice.

এই ৭টি খাবার আপনাকে ওজন কমাতে সাহায্য করবে

Coauthor of the study Dr. Daniel Wesson, of Case Western Reserve University in Cleveland, said while this study is at the proof-of-concept stage, biomarkers to identify early-stage Alzheimer’s may someday be pinpointed by identifying distinctive odor signatures.

The findings were published in the journal Scientific Reports.

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Scientists identify vital early warning of Alzheimer’s that could lead to improved treatment

Scientists made a breakthrough in identifying molecular mechanism by which Alzheimer’s destroys the ability for brain cells to “talk” to each other. The discovery could enable doctors to predict the onset of the disease years in advance, allowing crucial early treatment.

The lead researcher, Dr. Vladimir Sytnyk, from the University of New South Wales (UNSW) School of Biotechnology and Biomolecular Sciences, explains that loss of synapses - which connect brain neurons - is one of the first changes associated with Alzheimer's disease.

Loss of synapses is one of the early signs of the disease. Synapses connect neurons in our brain. Synapses are needed for all brain functions, especially forming memories and learning.

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Dr. Sytnyk says that synapses loss occurs in the very early stages of the degenerative disease, long before the nerve cells die, when only mild cognitive impairment is observed.

Alzheimer’s is a fast progressing neurodegenerative disease that starts out slow, but deteriorates over time. Short-term memory loss is the most common early symptom. Alzheimer’s is the most common cause of dementia, accounting for about 60-70% of all dementia cases.

German psychiatrist and pathologist Dr. Alois Alzheimer first discovered the disease in 1906. Dr. Alzheimer’s saw alterations in the post-mortem brain tissue of a woman who died of an unusual mental illness. Upon performing a post-mortem brain examination he found abnormal clumps what we now know as amyloid plaques and neurofibrillary tangles - now called tau tangles.

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Considered as the hallmarks of Alzheimer’s disease, these plaques and tangles are believed to cause the death of brain cells, which leads to the disease.

Age is one of the risk factors of Alzheimer’s. People over the age of 70 are at a higher risk of developing Alzheimer’s. Approximately 80 percent of people over the age of 85 are affected by this dreaded disease.

Short-term memory loss is the most common early symptom (Image credit: Creative commons)

Alzheimer’s has been recently ranked as the third leading cause of death in the United States. An estimated 5.3 million Americans of all ages have Alzheimer’s.

In UK, around 800,000 people are affected by the disease.

Dr. Sytnyk and his team wanted to further examine brain alterations related to Alzheimer’s. They studied a brain protein known as neural cell adhesion molecule 2 (NCAM2) – part of a group of molecules that connect synapse membranes, maintaining the synaptic connections between neurons.

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Researchers used brain tissue of dead people with or without the disease. They found that people with Alzheimer’s had low levels of synaptic NCAM2 in their hippocampus.

In the brain of Alzheimer’s patients, most of the damage occurs in the hippocampus of the brain, the area which is essential in forming memories.

Moreover, through mice studies, they discovered that NCAM2 was battered by beta-amyloid. As discussed earlier, bety-amyloid is the main constituent of the plaques that accumulate in the brains of Alzheimer’s patients.

The findings shows that the loss of synapses is related to the loss of NCAM2, caused by toxic effects of beta-amyloid, according to Dr. Sytnyk. He hints that it may open up a new avenue to study treatments that can stop the destruction of NCAM2.

The research team was made up of researchers from Neuroscience Research Australia (NeuRA) and the UNSW School of Medical Sciences’ Dementia Research Unit.

They publish their work the journal Nature Communications.

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Scientists discover possible solution for Alzheimer’s immunotherapy side effects

A team of researchers from the University of Southampton in England have discovered a potential solution for the side effects caused by immunotherapy treatment for Alzheimer’s.

Alzheimer’s disease is a chronic neurodegenerative disease. The disease starts out slow but progresses with age. Death of nerve cells in the brain causes Alzheimer’s. Symptoms include memory loss, impaired cognitive skills, difficulty speaking and decision-making.

Scientists believe plaques formed by beta-amyloid (pieces of protein) and neurofibrillary tangles in the brain causes the death of brain cells. In the patients with Alzheimer’s, the total size of the brain shrinks, while the tissue have constantly lesser nerve cells and connections.

The older you get, the higher is your risk of getting Alzheimer’s. People over the age of 70 are at a higher risk of developing Alzheimer’s. Around 80% people over the age of 85 are affected by this dreaded disease.

An estimated 46.8 million people globally have dementia and Alzheimer’s is the most common form of dementia.

Around 800,000 people are affected by Alzheimer’s in the UK.

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Immunotherapy is a hopeful approach for the treatment of Alzheimer’s. The procedure uses antibodies to prompt the immune system to discard beta-amyloid, which is a hallmark of Alzheimer’s disease.

Although, during test on lab mice, antibodies used against beta-amyloid have successfully cleared plaques and reversed cognitive loss, clinical trials showed side effects that caused inflammation in the brain of Alzheimer’s patients, especially ARIA (amyloid-related imaging abnormalities). ARIA causes small bleeding and threatening brain swelling.

The research team, led by Dr. Jessica Teeling, Associate Professor in Immunology at The Centre for Biological Sciences, engineered 3 antibodies to alter the process by which they engage cells in immune system. They discovered that small, explicit alterations in the anti-amyloid antibodies maintained the immunotherapeutic activity but didn’t have any inflammatory side effects.

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Dr. Teeling says it is crucial to learn more from studying these novel interventions and optimize their effects by using antibody engineering.

The findings of the study which was in collaboration with Lundbeck (a multinational pharmaceutical company based in Denmark), underscore the possibility of antibodies to terminate disease-causing plaques and suggest possible future treatments.

The researchers believe that further work should be done to increase potency of the antibody, but without the inflammatory side effects.

These studies give us a roadmap of how to use the advancements of antibody engineering and apply antibody therapeutics targeting various neurodegenerative diseases. In the future, Alzheimer’s drugs will possess new technologies and improvements to clear plaque buildup, while keeping unharmed other areas of the brain, concludes Dr. Stavenhagen of Lundbeck.

The study was printed in Acta Neuropathologica.

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Type 2 diabetes linked to neurofibrillary tangles found in brain cells of Alzheimer’s patients

A new study has found that people with type 2 diabetes who do not have dementia may be more prone to developing neurofibrillary tangles found in brain cells of Alzheimer’s patients. Tangles are abnormal collection of insoluble twisted fibers of a type of protein called Tau.

The study published in the journal Neurology was based on data from the US Alzheimer's Disease Neuroimaging Initiative. Scientists examined the link between type 2 diabetes and the death of brain cells and loss of connections. They also looked at the beta-amyloid plaques (protein fragment snipped from an amyloid precursor protein - APP) and protein tangles in the spinal fluid of the volunteers. Beta-amyloid plaques and neurofibrillary tangles found in brain cells of Alzheimer’s patients are the hallmark of Alzheimer’s disease described by Alois Alzheimer in 1906.

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The study involved 816 participants with an average age of 74. Of these participants, 397 individuals had mild cognitive impairment (MCI), 228 had no memory of cognitive problems, 191 were Alzheimer’s patients and 124 were diabetics.

The participants underwent MRI scan for the brain. Cerebrospinal fluid samples were taken from half of the participants to measure levels of beta-amyloid and tau – proteins that make up plaques and neurofibrillary tangles found in brain cells of Alzheimer’s patients.

The study found that the brain’s cortex of the people with type 2 diabetes were more thinning. Cortex is the area with the highest concentration of nerve cells. They also found higher levels of the protein tau in the spinal fluid of the patients with type 2 diabetes which indicated more tangles in the brain.

This study has proof that people with type 2 diabetes are at twice the risk of developing dementia, explains Dr. Velandai Srikanth, study author and an assoc. prof. at Monash University in Melbourne.

Studies like this one sought to understand how conditions such as diabetes may affect death of brain cells directly or indirectly. Since brain’s nerve cells do not restore themselves, it is really crucial to find ways to decrease brain cell death, he adds.

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However, Dr. Srikanth said that the study showed only a connection between type 2 diabetes and neurofibrillary tangles found in brain cells of Alzheimer’s patients. He wasn’t sure if type 2 diabetes was the cause. He pointed to high blood sugar and obesity which are common among people with type 2 diabetes. Other researches had linked obesity to a greater accumulation of tangles.

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“Obesity could be part of the puzzle, too …. There is an interesting body of evidence" tying obesity to tau, he explained,” said Dr. Srikanth.

Dr. Srikanth said that since the study analyzed participants’ data at only point in time, cause-and-effect association between diabetes and neurofibrillary tangles found in brain cells of Alzheimer’s patients was not determined.

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Awareness of memory problems may lessen 2 to 3 years before onset of memory loss or dementia

Researchers have found that people who develop dementia may start to lose awareness of their memory problems 2 to 3 years before memory loss or dementia starts.

Dementia is a general term for a decline in memory loss and cognitive skills with enough severity to interfere with daily life. The most common form of dementia is Alzheimer’s disease. An estimated 5.3 million Americans of all ages have Alzheimer’s. It is the sixth leading cause of death in the United States. According to Alzheimer’s Society UK, the number of Alzheimer’s patients in UK will reach 850,000 by the end of this year.  

The study done by Rush University Medical Center in Chicago was published in the journal Neurology.

The researchers also found that many memory loss or brain changes related to dementia, or pathologies are to be blamed for the deterioration in memory awareness.

Robert S. Wilson, PhD, of Chicago’s Rush University Medical Center, says that their findings suggest not being aware about one’s memory problems is an unavoidable characteristic of late-life dementia that is initiated by an accumulation of changes in the brain that are related to dementia.

Dr. Wilson, who is also a study author added that not being aware of memory loss is usual in dementia, but they never knew much about its commonness, when it develops and why some individual appear more affected than others.

Participants in the memory loss or dementia study were 2,092 adults with an average age of 76 years, who had no signs of memory loss or cognitive impairment. Researchers monitored the participants for more than 10 years. They had to take yearly tests on memory and cognitive skills. They were asked how often they found it difficult to remember things and were also told to assess their memory compared to ten years prior.

During the course of the study, 239 participants were diagnosed with dementia. In these seniors, awareness of memory problems began to drop abruptly on an average of 30 months before dementia first appeared. While results were same for all the participants, researchers were surprised to find that memory loss occurred earlier in younger participants compared to the older ones. Researchers believe that this might be because reporting was misrepresented in older people who usually expect memory loss as a usual part of aging.

Although there were distinct differences in the timing of the unawareness and the speed of its progression, almost all the people were unaware about their memory difficulties at any point in the disease, explains Dr. Wilson.

Brains of 385 subjects who died during the study period were also examined by the researchers. They assessed these brains for seven types of brain alterations that are common to dementia. They discovered that three dementia-related pathologies were linked with the speedy degeneration in memory:

1.       Tau proteins also known as tangles

2.       Infarcts (areas of brain damage)

3.       Changes in the TDP-43 protein  

As these changes in the brain build up, people fail to realize that their memory is declining.

This study highlights the usefulness of loved ones and family members asking for help from healthcare professionals and doctors getting information from family or friends during the decision making process about whether someone has dementia, since those affected by dementia may not be able to provide decisive information about the case study of their own cognition, says Dr. Wilson.

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