Dementia Caregivers Want Robots for Joy and Sorrow to Take Care of Patients

Example of one of the robots designed by caregivers (Image Credit: Healthcare Robotics Lab/University of California San Diego)

A bit of robotic assistance can help people with dementia and their caregivers. Robots current available for the elderly help them around the house but there aren’t many robots that assist people with dementia. So, researchers at the University of California, San Diego wanted to find out what kinds of robots would actually help. They spent six months co-designing robots with informal caregivers for people with dementia, such as family members. 

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They found that caregivers wanted the robots to fulfill two major roles: support positive moments shared by caregivers and their loved ones; and lessen caregivers' emotional stress by taking on difficult tasks, such as answering repeated questions and restricting unhealthy food.


“Caregivers conceived of robots not only managing difficult aspects of caregiving -- but also for supporting joyful and fun activities,” said Laurel Riek, a professor of computer science at UC San Diego, and the paper's senior author.


For the study, the research team led by Riek built relationships with three different dementia day care centers in San Diego County, reportsUC-San Diego.

Image: Creative commons

Researchers conducted a series of interviews and hands-on workshops with caregivers.

• Based on the results of the six-month long community design process, the team identified various characteristics and designs a robot should have to support the caregivers and patients with dementia:
• Robots should help redirect conversations when repetitive questioning becomes burdensome
• Robots should be integrated into everyday objects that the people with dementia are already familiar with, or borrow features from those objects.
• Robots should be able to adapt to new situations and to the behavior of the person with dementia.
• Robots should be able to learn from end users, and customize and personalize their interaction and responses.
• Robots should have human-like components. That is not to say that they should look human. Rather the machines could, for example, use a real human voice or face.

·       Robots should have human-like components. That is not to say that they should look human. Rather the machines could, for example, use a real human voice or face.

Read more ScientistsReport Significant Breakthrough in Anti-Aging

The researchers presented their findings at the Human Robot Interaction conference in South Korea.

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Poor sleep increases Alzheimer’s brain proteins

A single night of poor sleep can cause a spike in brain proteins linked to Alzheimer’s disease, a new study reports.

Researchers from the U.S. and the Netherlands have found that sleep helps the body clear away two compounds in the brain, called amyloid and tau, and interrupted, poor sleep may cause too much of them to build up.

While the study doesn't show that poor sleep causes Alzheimer's, it adds one more piece to the puzzle of what causes dementia. [Read more Study:Access to nature makes men and seniors sleep better]

The team believes that the findings back the notion that chronic poor sleep in midlife could elevate the risk of developing Alzheimer's later in life.

Read more Does Memory Loss Always Mean Dementia?

“When people had their slow-wave sleep disrupted, their amyloid levels increased by about 10 percent,” says study leader Dr. Yo-El Ju of Washington University in St. Louis.

Although scientists knew there was a connection between dementia and poor sleep, it wasn’t clear whether dementia was driving insomnia or vice versa.

The study was jointly conductedby researchers from Washington University School of Medicine in St. Louis; Stanford University in California, in the U.S., and Radboud University Medical Centre in the Netherlands.

Alzheimer’s disease is a neurodegenerative disease that progresses rapidly. It is the most common cause of dementia, accounting for about 70% of all dementia cases. The disease affects memory, decision-making, language, thinking, and speech.

The brains of people with Alzheimer's disease feature two hallmarks of the disease – plaques of amyloid protein and tangles of tau protein. These plaques and tangles causes neuron cells to die.

In the UK, around 850,000 people are currently living with dementia, and the majority have Alzheimer’s disease, for which there is no cure. Although the number of dementia cases is dropping as people adopt healthier lifestyles, the number of people living with the illness is expected to rise to 1.2 million by 2040 because of the ageing population. [Read more Whatcauses aging? Can the process be slowed?]

More than a third of Britons also sleep for less than 6 hours a night, according to The Sleep Council.

For their study, the researchers sought to identify the most important phase of sleep.

“What we did was allow people to sleep a normal amount of time, but we prevented them from getting deep sleep or what is called slow-wave sleep,” Ju told NBC News.

“When we interrupted just the slow-wave sleep part, they still had an increase in amyloid. So this tells us it's getting the deep slow-wave sleep that's important for reducing the levels of amyloid.”

Ju and colleagues recruited 22 healthy adults aged between 35 and 65. All the participants reported experiencing no sleep problems and had no cognitive impairments.

The participants showed up in a controlled sleep lab. Half were allowed to sleep normally, while the other half were constantly kept in shallow sleep. [Read more Newprotein target may reverse memory loss in Alzheimer’s]

“As soon as they got into slow-wave sleep, they got a beep. And the beeps got louder and louder and louder until they came out of the deep sleep,” says Prof. Ju.

“It was pretty harsh.”

The participants didn’t realize their sleep had been interrupted, and this went on for the entire night.

The participants’ spinal fluid was analyzed in the morning.

“When people had their slow wave sleep disrupted, their amyloid levels increased by about 10 percent,” Prof. Ju says.

The subjects were also fitted with sleep monitors to measure theirsleep at home. Participants who experienced poor sleep at home were found to have higher levels of a second Alzheimer’s related protein called tau. [Read more Scientistsreport significant breakthrough in anti-aging]

Prof. Ju says they were not surprised to see that tau levels didn’t increase after only one night of poor sleep whereas this did cause amyloid levels to rise, since tau levels tend to change more slowly.

“But we could see, when the participants had several bad nights in a row at home that their tau levels had risen,” she adds.

Prof. Ju concludes by saying:

“At this point, we can't say whether improving sleep will reduce your risk of developing Alzheimer's. All we can really say is that bad sleep increases levels of some proteins that are associated with Alzheimer's disease. But a good night's sleep is something you want to be striving for anyway.”

Next, the team plans to study whether treating obstructive sleep apnea will improve people's slow-wave sleep and affect amyloid levels. Sleep apnea is a common cause of sleep disruption. People with this condition have a higher risk of developing dementia.

The study was published in the journal Brain.

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Family History of Alzheimer’s May Explain Link of Metabolic Gene that Raises Risk for Disease

Years of conflicting research that failed to pinpoint the missing link between a mitochondrial gene and the risk of Alzheimer’s may have finally been resolved by the scientists of Iowa State University (ISU) in the U.S. The researchers say that family history of Alzheimer's disease may be the missing link. It shows that having a family history of Alzheimer's disease appears to alter the behavior of the gene called TOMM40.

Lead researcher AurielWillette, assistant professor of food science and human nutrition at ISU, says the initial discovery of the gene TOMM40 gave the scientists impression that it raises the risk of Alzheimer’s. But the findings were later dismissed when several studies failed to replicate the results.

However, Willette and his colleagues weren’t convinced that the gene was a total failure, so they decided to examine other elements that may be producing the mixed results.

The researchers discovered a startling difference in the gene’s effect on cognitive function, memory and risk based on a family history of Alzheimer’s disease and the length of a specific part of the gene.

“It was kind of a shot in the dark, but we found if you don’t have a family history of Alzheimer’s disease, then having a longer version of the gene is a good thing. It is related to better memory up to 10 years later and about one-fifth of the risk for developing Alzheimer’s disease,” said Willette, who is also an adjunct assistant professor of neurology at the University of Iowa.

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“However, if your mom or dad has Alzheimer’s, then having a long version is bad. It’s a complete polar opposite.”

The main pathological hallmarks ofAlzheimer’s disease are amyloid-β (Aβ) plaques, and neurofibrillary tangles, caused by tau protein. These plaques and tangles around the neurons eventually cause the neurons to die.

Outward symptoms start with mild memoryloss. As the symptoms progress, the person finds it increasingly difficult to hold a conversation or carry out everyday tasks such as button a shirt.

Although numerous studies being conducted worldwide are providing new clues, scientists still do not know the exact causesof Alzheimer's disease. They think that there are various factors, and some of these affect different people in different ways, according to the study.

Family history of Alzheimer’s and TOMM40

The researchers designed the study to explore the magnitude to which family history regulated the effects of TOMM40 on symptoms of Alzheimer's disease, such as thinking and memory loss.

They used data from two large studies of Alzheimer's disease. One set of data came from 912 adults in the Wisconsin Registry for Alzheimer's Prevention – a study which is following middle-aged adults at risk of developing Alzheimer's and following changes in cognitive function and memory loss, based on assessments carried out every 2 years for up to a decade.

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The other set of data came from 365 participants in the Alzheimer's Disease Neuroimaging Initiative – a study which is monitoring similar changes in older adults with and without the disease.

The researchers found that having a family history of Alzheimer's disease appears to make a big difference in how TOMM40 affects memory and thinking, and that the difference depends on the length of a particular portion of the gene. [Read more Study:Access to nature makes men and seniors sleep better]

Prof. Willette and his team found that having the longer version of the gene, together with no family history of Alzheimer's, was linked to around a one-fifth lower risk of developing Alzheimer's disease and better memory up to 10 years later.

Family history was focused particularly on whether Alzheimer’s disease was found in a participant’s parents. The researchers also discovered a link between the family history, gene, and mitochondrial function, which produces energy to power the cells. Age, gender and education were controlled for in the examination of TOMM40 gene and family history in the participants.

The team is also involved in another project which is investigating factors that affect how the body makes and uses energy, such as insulin resistance, as well as proteins and enzymes that affect energy regulation.

Studies like these are slowly uncovering what happens to thinking and memory when there is not enough energy for brain cells to perform properly.

The study was published in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association.

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What is Alzheimer’s Disease and How is it Treated?

Alzheimer’s disease is a progressive neurological disorder that causes brain cells to degenerate, resulting in memory loss and cognitive decline. It is the most common form of dementia, accounting for 60 to 80% of dementia cases in the U.S. Symptoms of Alzheimer’s usually develop slowly, but get worse over time, and at the end stage the patient forgets how to perform daily tasks such as wearing a shirt or going to the bathroom.

Statistics

Alzheimer’s is the 6thleading cause of death in the U.S. More than 5 million Americans are living with Alzheimer’s disease. The number is believed to rise to nearly 14 million by 2050. Every 65 seconds, someone in the U.S. develops Alzheimer’s.

Globally, every 3 seconds someone develops dementia. In 2015, an estimated 46.8 million people worldwide were living with dementia and this number is projected to rise to 50 million in 2017. Much of the increase will be in developing countries. Low and middle-income countries already have 58% of dementia cases worldwide. China, India, and other South Asian countries will see a dramatic rise in dementia cases because these countries are seeing the fastest growth in their elderly population.

A Short History

Dr. Alzheimer (left), his patient Auguste Deter (right)

The disease is named after German psychiatrist Alois Alzheimer, who first described it in 1901. During the 1890s, Dr. Alzheimer had a female patient named Auguste Deter. Fifty-year-old Deter was showing signs of dementia. She also had trouble sleeping, and she’d drag sheets across the house, and scream for hours in the middle of the night. Deter was admitted to a mental institution in Frankfurt, Germany. When Dr. Alzheimer would ask her to write her name, she’d forget her name and repeat, “I have lost myself.” When she was put in an isolation room for a while and later released, she ran out screaming, “I will not be cut. I do not cut myself.” Dr. Alzheimer called it the “Disease of Forgetfulness.” Deter died in 1906 of “sepsis caused by an infected bedsore” in 1906. Alzheimer decided to examine her brain and upon examination he discovered senile plaques and neurofibrillary tangles. These are the hallmarks of Alzheimer’s disease.

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What Causes Alzheimer’s?

Like all types of dementia, Alzheimer's disease is caused by brain cell death.

Beta Amyloid Plaques

In Alzheimer’s disease amyloid plaques accumulate between nerve cells (neurons) in the brain. Amyloid is a general term for protein fragments thatour body produces naturally. Beta amyloid is a protein piece clipped from an amyloid precursor protein (APP). In the brain of a healthy person, these pieces of protein are broken down and removed. But in Alzheimer's disease, these fragments are not eliminated and they amass to form solid, insoluble plaques.

Neurofibrillary Tangles

These are insoluble twisted fibers found inside the cells of the brain. A protein called tau is the main component of these tangles. Tau builds part of a structure called a microtubule, which aids in transporting nutrients and other vital substances from one part of the nerve cell to another. Inside the brain of Alzheimer's disease patient, the tau protein is abnormal and the microtubule formations collapse.

What are the Risk Factors for Alzheimer’s?

Age. Increased age is the biggest risk factor for Alzheimer’s disease. For most people with Alzheimer’s, they get it after age 65.

Family history. People who have a parentor sibling with Alzheimer’s are more likely to develop the disease.

Gender. Women are at greater risk of developing the disease than men. Out of the 5 million people living with Alzheimer’s in the United States, 3.2 million are women.

Genes. Genes play a big role in the development of Alzheimer’s. According to scientists, two categories of genes – risk genes and deterministic genes – influence whether a person develops a disease. Alzheimer's genes have been found in both categories.

Down syndrome. Scientists do not know why, but people with Down Syndrome often get Alzheimer's disease in their 30s and 40s.

Head injury. Some studies have found a link between Alzheimer's disease and a major head trauma.

Other factors. High cholesterol in blood and high blood pressure may also raise the risk of developing Alzheimer’s disease.

Early-onset Alzheimer’s

Early-onset Alzheimer's can affect younger people with a family history of the disease, normally between the ages of 30 and 60 years. Less than 5% of all Alzheimer’s cases are early-onset.

What are the Symptoms of Alzheimer’s?

The early signs of Alzheimer’s may be forgetting recent events or conversations. The progression of the disease causes the person to develop severe memory impairment, which makes them unable to carry out simple everyday tasks. However, it should be noted that loss of memory doesn’t always mean dementia.

Symptoms of Alzheimer’s disease may include:

• Misplacing personal belongings
• Repetitive questions or conversations
• Getting lost in familiar surroundings
• Forgetting appointments orevents
• Lack of understanding of safety risks
• Unable to make decisions or poor decision-making ability
• Inability to oversee finances
• Inability to recognize faces
• Difficulty finding common words while conversing
• Inability to use simple tools
• Impaired speaking, writing and reading
• Errors in writing, spelling and speaking
• Mood changes, including agitation, apathy and social withdrawal
• Compulsive, obsessive, or socially unacceptable behavior
• Loss of empathy

What are the Stages of Alzheimer’s?

Alzheimer's progression can be broken down into 3 main stages:

Preclinical. It is the stage before symptoms appear

Mild cognitive impairment. Symptoms are mild at this stage

Dementia. This is the stage when the person is believed to have dementia

How is Alzheimer’s Diagnosed?

There is no single test for Alzheimer's, so doctors usually do a check on the person's medical history, history from relatives, and behavioral observations before making a diagnosis. Computed tomography (CT) or magnetic resonance imaging (MRI), Single-photon emission computedtomography (SPECT) or positron emission tomography (PET) are standard procedures, which help to exclude other cerebral pathology or subtypes of dementia.

The person's neurological function may also be checked. It may be done by testing their senses, balance, and reflexes.

Other tests may include a blood or urine test etc.

Sometimes the dementia symptoms may be linked to an inherited disorder such as Huntington's disease, so doctors may do a genetic testing.

Cognitive Assessment

To do a cognitive assessment, the doctor may ask the person following questions:

• What is your first name and last name?
• What is your age?
• What is your spouse’s name?
• What is your date of birth?
• What is the time, to the nearest hour?
• Can you recognize two people, for example, the doctor, nurse, or caregiver?
• What year is it now?
• In which year did (WW II) happen?
• What is the name of the hospital or town we are in?
• Who’s the president?
• Count backward from 20 down to 1

What are the treatments for Alzheimer’s?

There is no known cure for Alzheimer's. Scientists cannot reverse the death of brain cells.

However, therapeutic interventions may ease the symptoms of the disease.

Is Alzheimer’s Preventable?

Alzheimer's isn’t a preventablecondition. But a range of lifestyle risk factors for the condition can be modified. Studies have found that changes in diet, exercise and habits – steps to lower the risk of cardiovascular disease – may also reduce one’s risk of developing Alzheimer's disease and other disorders that cause dementia. The following lifestyle choices may reduce the risk of Alzheimer's:

• Exercise regularly
• Eat lots of fruits and vegetables, healthy oils and foods low in saturated fat
• Follow guidelines to manage diabetes, high blood pressure, and high cholesterol
• Do not smoke

Studies have shown that creating art, participating in social events, reading, playing board games, dancing, playing an instrument, and other activities that require mental activity and social engagement may help keep dementia at bay.

Famous People with Alzheimer’s

Jimmy Stewart in "It's a Wonderful Life"

• Malcolm Young (1953 – 2017). Legendary guitarist of AC/DC
• Glenn Campbell (1936-2017). Country singer and guitarist
• Perry Como (1912-2001). Singer, TV personality
• Charles Bronson (1921 — 2003). Actor, famous for “Deathwish” movies
• Ronald Reagan (1911 – 2004). US president
• Charlton Heston (1923 – 2008). Legendary actor
• Norman Rockwell (1894 – 1978). Famous painter
• Rita Hayworth (1918 – 1987). Famous actress
• Sugar Ray Robinson (1921 – 1989). Famous boxer
• Estelle Getty (1923 – 1998). Actress well-known for “Golden Girls”
• Peter Falk (1927 – 2011). Actor, best known for TV series “Columbo”
• James Stewart (1908 – 1997). Legendary actor famous for “It’s a wonderful life,” “Mr. Smith goes to Washington,” and many other movies
• Rosa Parks (1913 – 2005). Civil rights activist known as “the Mother of the Freedom Movement”
• Robin Williams (1951 – 2014). Famous actor. Although Williams was thought to have Alzheimer’s, it was revealed after his death that he wassuffering from Lewy Body Dementia.
• Casey Kasem (1932 – 2014). Famous for America’s Top 40 Countdown

If you have a loved one who you think might have Alzheimer’s, you may seek help by contacting Alzheimer’s helpline.

Families of Alzheimer’s patients can seek help from senior care referral services such as A Place for Mom to receive care options that’s a good match for their family.

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Alzheimer’s memory loss may be reversed by blocking a key enzyme

Targeting an enzyme that interferes with memory-forming processes in Alzheimer’s patients can be an effective treatment for memory loss, according to a new study. A team of scientists from the Massachusetts Institute of Technology (MIT) in the U.S. found that it may be possible to reverse Alzheimer’s related memory loss with drugs that selectively impede the ability of the Histone deacetylase-2 (HDAC2) enzyme to interfere with the communication between brain cells.

Previously, scientists failed to target HDAC2because the drugs that were used also impeded other roles of the enzyme, causing toxic side effects.

The new research has shown that blocking a molecule called sp3 that binds to HDAC2 might effectively stop them both from disrupting the communication between brain cells that is crucial for memory.

"If we can remove the blockade by inhibiting HDAC2 activity or reducing HDAC2 levels," explains Seniorauthor Prof. Li-Huei Tsai, director of the Picower Institute for Learning and Memory at MIT, "then we can remove the blockade and restore expression of all these genes necessary for learning and memory."

For over a decade, Prof. Tsai has been researching the role that enzymes called HDACs play in memory loss. In2007, she discovered that blocking HDAC activity in mice could reverse memory loss. There are around a dozen types of HDAC in humans.

Alzheimer's disease is the most common form of dementia, affecting around 850,000 people in the UK. This neurodegenerative disease gradually diminishes a person’s ability to remember, think, reason, and make decisions.

There is no cure for thedisease and scientists do not know the causes of the disease. It is more common among people over 60 years, but it can affect younger people as well.

The new study focuses on the disruption of a process called synaptic plasticity, which is thought to be crucial for memory and learning.

Research has revealed that synapses – the connections between brain cells – are "plastic" and are not fixed as the soldered joints in electronic circuits.

Scientists define synaptic plasticity as a biological process whereby synapses change over time, depending on specific patterns of activity.

Read more Exercise may protect against cognitive decline

Scientists previously tested compounds that inhibit HDAC2, but most these produced side effects, such as interfering with HDAC1. HDAC1 is crucial for cell proliferation, especially in red and white blood cells.

Therefore, in this new study, Prof. Tsai and his team sought to find a way to target only the HDAC2 activity that impedes memory. The team searched for proteins that help the enzyme to bind to the relevant genes.

To find the diabolical pairing, the researchers examined the expression of genes in postmortem brain samples taken from people who didn’t have Alzheimer’s.

Of these samples some brains had high and some had low levels of HDAC2, which helped the researchers to identify more than 2,000 genes that might be involved with HDAC2 activity.

Next, a technique called gene knockdown was used to prevent the expression of HDAC2 and other genes in mice. This narrowed down the search to a gene that made the protein Sp3.

Fragments of HDAC2 were used to connect with Sp3 in the mice. This effectively mopped up the proteins and prevented them from forming a complex with complete HDAC2 enzymes.

This clean-up was useful and it helped restore mice’s nerve functions, providing evidence that the enzyme and its helper were both required to latch onto the histones and DNA and prevent them from working.

The study was published in the journal Cell Reports.

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Does Memory Loss Always Mean Dementia?

Dementia or senility isn’t a specific disease. Instead, it is a broad category of symptoms that affect the brain and causes memory loss. The loss of memory affects social abilities and cognitive skills that are severe enough to interfere with daily life.

The most common form of dementia is Alzheimer’s disease, which accounts for 60%-80% of all dementia cases. Other common types of dementia include vascular dementia – accounting for 25%, Lewy body dementia – accounting for 15% and frontotemporal dementia. A person can be affected by more than one type of dementia.

Every 3 seconds, someone in the world develops dementia. There were an estimated 46.8 million people worldwide living with dementia in 2015 and this number is believed to be close to 50 million people in 2017. 5.2% of people over the age of 60 are living with dementia globally. The number of people with dementia will almost double every 20 years, reaching 75 million in 2030 and 131.5 million in 2050. Developing countries will see much of theincrease. Currently, around 58% of people with dementia live in low- and middle-income countries, but this will rise to 68% by 2050. The fastest growth in the elderly population is taking place in China, India, and their south Asian and western Pacific neighbors.

There are about 5.7 million people of all ages are affected with Alzheimer’s disease in the USA. Almost two thirds of Americans with Alzheimer’s are women.

According to Alzheimer’s Society, UK, an estimated 850,000 people are affected by dementia in the UK, with the number expected to rise to over 1 million by 2025. It is expected that 225,000 people will develop dementia this year that is 1 person every 3 minutes.

Does Memory Loss Mean A Person Has Dementia?

Although loss of memory usually occurs in dementia, loss of memory alone does not mean a person has dementia. People lose some degree of memory as they get older. Naturally occurring memory loss isn’t considered dementia. At least 2 of thefollowing cognitive functions must be significantly damaged to be considered dementia:

1. Loss of memory
2. Problem communicating or understanding language
3. Inability to focus
4. Inability to make decisions or judgments
5. Lack of visual perception

What are the Types of Dementia?

The different types of dementia include:

• Alzheimer’s disease. It is the most common for of dementia, accounting for 60 to 80 percent of all dementia cases. Alzheimer’s causes problems with memory, thinking and behavior.
• Vascular dementia. It is the second most common type of dementia, which occurs after a stroke.
• Dementia with Lewy Bodies (DLB). It is a form of progressive dementia that leads to a decline in thinking, reasoning and independent function due to abnormal microscopic deposits that damage brain cells over time.
• Parkinson’s disease dementia. It is a cognitive impairment that ultimately affects many people with Parkinson's disease.
• Mixed dementia. In this type of dementia, abnormal characteristics of more than one type of dementia occur simultaneously.
• Frontotemporal dementia (FTD). It is a group of disorders caused by progressive nerve cell loss in the brain's frontal lobes (the areas behind the forehead) or its temporal lobes (the regions behind the ears).
• Huntington’s disease. It is a progressive brain disorder caused by a defective gene. This disease causes changes in the central area of the brain, which affect movement, mood and thinking skills.
• Creutzfeldt-Jakob disease (CJD). It is the most common human form of a group of rare, fatal brain disorders known as prion diseases.
• Normal pressure hydrocephalus (NPH). It is a brain disorder in which excess cerebrospinal fluid accumulates in the brain's ventricle, causing thinking and reasoning problems, difficulty walking, and loss of bladder control.
• Wernicke-Korsakoff Syndrome. It is a chronic memory disorder caused by severe deficiency of thiamine (vitamin B-1). Korsakoff syndrome is most commonly caused by alcohol misuse, but certain other conditions also can cause the syndrome.
• Posterior cortical atrophy (PCA). It is the gradual and progressive degeneration of the outer layer of the brain (the cortex) in the part of the brain located in the back of the head (posterior).

Are there Warning Signs One Should Watch Out For?

What Are the Stages of Dementia?

Dementia may have several stages such as, mild, moderate or severe. A dementia patient may fall into 2 different stages at once. Progression of a patient’s condition cannot be determined by the stages of dementia. A patient may remain in a particular stage for a few months or a several years. Progression of the disease varies in patient to patient.

What Are the Causes of Dementia?

Death of the nerve cells in the brain causes dementia. Dementia may be caused by head injury, stroke or a brain tumor. Since, death of brain cells may occur in different parts of the brain, dementia’s affect on people may vary from person to person.

What Are the Signs and symptoms of Dementia?

Dementia, in its early stage may have signs like forgetting things, difficulty performing tasks that were previously done without effort, losing common items such as keys, glasses etc. Difficulty learning new things is a very common early sign of dementia. Many Alzheimer’s patients or patients with other forms of dementia are unaware about their problems. The behavioral changes become evident with the progression of the disease. Patients fail to perform simple tasks, such as putting on clothes or going to the bathroom. Some patients may forget their phone numbers, addresses or their date of birth. They may be unaware about their surrounding environment. Some patients may forget to take their food, which may lead to marked weight loss. At the late stages of dementia, patients often cannot recognize their friends or family members. They lose their ability to communicate effectively. They become unable to care for themselves and need help of others to perform daily activities. As the disease progresses, patients start to forget how to walk or how to get up from a chair.

Can Dementia Be Reversed?

Doctors may identify the causes of certain dementia, therefore conditions can be reversed with proper treatment.

• When dementia-like conditions occur from fever or other infections such as meningitis, encephalitis, syphilis, Lyme disease. Dementia from immune disorders such as leukemia and multiple sclerosis can also be reversed.
• Dementia from metabolic problems and abnormalities of endocrine.
• When nutritional deficiencies cause dementia.
• When dementia is caused by poisoning.
• Subdural hematomas
• Rarely, brain tumors can cause dementia
• Reactions to medication

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Oral health may be linked to cognitive decline

According to new research published in the Journal of the American Geriatrics Society, there may be a link between oral health and the progression of cognitive decline.

"Clinical evidence suggests that the frequency of oral health problems increases significantly in cognitively impaired older people, particularly those with dementia,” said lead researcher Bei Wu, PhD, of Duke University's School of Nursing in Durham, North Carolina in the US.

"In addition, many of the factors associated with poor oral health — such as poor nutrition and systemic diseases like diabetes and cardiovascular disease — are also associated with poor cognitive function,” he added.

The researchers caution, however, that more studies are needed.

Findings came from the first systematic review of studies focused on oral health and cognition. These two important areas of research are important because in a growing older adult population, some 36% of people over age 70 are already living with some degree of cognitive decline. Researchers believe that a common inflammatory pathway may hold the key to a link between oral hygiene and cognitive impairment, if such a link exists.

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Poor oral health has been blamed for heart disease, due to the spread of bacteria and oral health problems may be aggravated by diabetes and HIV/AIDS due to reduction of body’s resistance to infection.

Alzheimer's Association estimates around 5.4 million people in the US have Alzheimer's disease - the most common form of dementia.

To look for a link between oral health and cognitive status, Dr. Wu and her colleagues combed through 56 studies published between January1993 and March 2013 that examined the relationship between oral health and change in cognitive health or dementia incidence. They analyzed relevant cross-sectional (data collected at one specific point in time) and longitudinal (data collected over an extended period of time).

Some of the studies analyzed found that dental health measures, such as the number of teeth, the number of cavities, and the presence of gum disease, were linked to an increased risk of cognitive decline or dementia. Which is interesting considering a 2013 study found gum disease bacteria in the brains of Alzheimer’s disease patients — but this study in no way proved that gum disease causes Alzheimer’s disease. It just acknowledged an association.

However, researchers involved with the current review also noted that the findings based on the number of teeth or cavities are conflicting, and limited studies suggested that the dental conditions such as gingivitis are associated with cognitive decline. Similarly, the team didn’t regularly find that cognitive decline was associated with greater loss of teeth or number of decayed teeth. However, it is likely that "methodological limitations play a major role in explaining the inconsistent findings," they wrote.

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"There is not enough evidence to date to conclude that a causal association exists between cognitive function and oral health. For future research, we recommend that investigators gather data from larger and more population representative samples, use standard cognitive assessments and oral health measures, and use more sophisticated data analyses," Dr. Wu said.

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People with rosacea are at higher risk of Alzheimer’s

According to a new study people with rosacea – the facial redness affecting millions of people – are at an increased risk of developing dementia, particularly Alzheimer's disease, compared with people without the condition. The study also found that older patients and patients who were diagnosed by a hospital dermatologist were at the highest risk of developing Alzheimer’s.

However, the researchers were quick to point out that people with rosacea should not be overly concerned about the finding.

“It is important for patients to remember that having rosacea does not guarantee that they will develop Alzheimer’s disease,” said lead author Dr. Alexander Egeberg of the department of dermato-allergology at Herlev and Gentofte Hospital, in Copenhagen, Denmark.

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“In fact, while the risk in rosacea patients may be slightly increased compared with the general population, the absolute risk [to any one patient] is still quite low,” he said.

Rosacea is very common, where some estimates suggest up to 1 in 10 people may have it. According to the National Rosacea Society, approximately 16 million Americans suffer from it. Around 1 in every 600 people in the UK are diagnosed with the condition each year. It most commonly affects people with fair skin, but can also occur in people of Asian and African origin. The condition is often mistaken for eczema, acne, or some other skin condition. Rosacea occurs in both men and women, but tends to be more common in women. Most cases are first diagnosed in people aged 30 to 50. There are no cures for the condition, but some medicines can alleviate symptoms.

The study was conducted by the team because there is evidence rosacea is linked with higher levels of certain proteins that have also been implicated in various neurological disorders, such as Alzheimer's disease and other forms of dementia. The proteins in question here are matrix metalloproteinases and antimicrobial peptides.

For the new study, Dr. Egeberg’s team analyzed data from the Danish nationalhealth registry system covering the period 1997-2012. The nation’s entire population – nearly 6 million men and women – were included, out of whom 83,500 had rosacea.

Individuals were followed until December 31, 2012, migration, a diagnosis of dementia, or death from any cause, whichever came first. Altogether, just over 99,000 developed dementia, including around 29,000 who were diagnosed with Alzheimer's disease.

After analysis, researchers found that people with rosacea had a 7% increased risk of dementia and a 25% increased risk of Alzheimer’s, compared with patients who did not have the skin condition. Older people were at higher risk.

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The results also varied between men and women, where women with rosacea were at 28% increased risk of Alzheimer’s and men were at 16% increased risk.

For women, the raised risk of Alzheimer's linked to rosacea was 28 percent, whereas for men with the skin disorder it was 16 percent.

When the analysis was limited to cases of rosacea that had been diagnosed by a hospital dermatologist, the researchers found the increased risk of dementia was 42%, while the risk was 92% for Alzheimer’s disease.

Dr. Egeberg says:

"A subtype of patients have prominent neurological symptoms such as burning and stinging pain in the skin, migraines, and neuropsychiatric symptoms, suggesting a link between rosacea and neurological diseases."

"Indeed," he continues, "emerging evidence suggests that rosacea may be linked with neurological disorders including Parkinson's disease and now also Alzheimer's disease."

He says that the risk may be explained by certain underlying mechanisms shared by rosacea and Alzheimer's disease, but it is no known whether one causes the other.

The team suggests doctors should look out for symptoms of cognitive impairment in older patients with rosacea, and that only further studies can affirm if treating rosacea may also improve patients' risk of developing dementia.

The findings are published in the Annals of Neurology, a journal of the American Neurological Association and Child Neurology Society.

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Belly Fat May Cause Cognitive Impairment

A team of scientists from 3 Irish universities – St. James's Hospital and Trinity College Dublin, both in Northern Ireland, and Nutrition Innovation Centre for Food and Health at Ulster University – found that having higher levels of belly fat in old age is associated with a decrease in cognitive function.

Prevalence of Alzheimer’s and other forms of dementia is growing with the rise in average age of population. Currently, an estimated 47 million people worldwide are affected by dementia. This number is expected to rise to 75 million by 2030.

Scientists are trying to understand the risk factors involved in dementia as it will help us with potential interventions to lower the risk of this condition developing as we age. One such risk factor is obesity.

Earlier studies have shown that overweight or obese adults do not perform as well on tests of memory and visuospatial ability compared to those who are a normal weight. However, researchers aren’t sure if this trend continues into older age.

While previous studieshave looked into this matter, the results produced were contradictory. Since each study involved different forms of cognitive test, it is difficult to conduct a meta-analysis with the pooled results.

For this new study, the researchers set out to answer this question more conclusively using a large-scale trial. [Read more High-fat diet damages brain, affecting learning and memory]

The scientists from the three universities used data from the Trinity Ulster Department of Agriculture aging cohort study, which is a cross-border collaborative research project gathering data from thousands of adults over the age of 60 in Northern Ireland and Ireland.

Each of the 5,186 participants was assessed using a number of cognitive tests.

The team found that a higher waist to hip ratio was linked with reduced cognitive function. This could be due to an increased secretion of inflammatory markers by belly fat, which in previous studies had been linked with a higher risk of cognitive impairment.

On the contrary, bodymass index (BMI) measurements did not show the same trend; in fact, higher BMI was found to protect cognitive function. Researchers believe this is because BMI is a crude measure of body fat and cannot differentiate between fat and fat-free mass (muscle); it only takes into account weight and height.  

How cognition is influenced by belly fat?

Researchers believe that belly fat's impact on cognition might be due to high secretion of inflammatory markers – particularly C-reactive protein. This chemical is produced when fat cells send out signals. Increased levels of this have previously been linked to cognitive decline.

It should also be noted that according to studies, levels of inflammatory markers in the blood increases in the lead-in to dementia, before symptoms appear. 

Hemoglobin A1C (HbA1C) is another molecule that seemed crucial. When during their analysis, the researchers controlled for levels of HbA1C, the significant effect of belly fat on cognition disappeared.

The prevalence of obesity and dementia are putting enormous burdens on the society. Studies like this are crucial because by reducing obesity we may be able to curtail the prevalence of dementia.

The findings are published in the British Journal of Nutrition.

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New implantable capsule for Alzheimer’s prevention

In a breakthrough Alzheimer’s treatment, scientists from the Ecole Polytechnique Federale de Lausanne (EPFL) in Switzerland have developed an implantable capsule that works by turning the patient's immune system against the disease. The lab of Patrick Aebischer at EPFL developed this bioactive capsule which contains cells that have been genetically engineered to produce antibodies against amyloid-β.

When German psychiatrist and pathologist Alois Alzheimer described Alzheimer’s disease for the first time in 1906, he brought to light the presence of two types of lesions in the brain – Senile plaques and Neurofibrillary tangles. Senile plaques are caused by over-accumulation of the protein Amyloid beta (amyloid-β) in different parts of the brain.

The capsule, when implanted under the skin, releases antibodies that travel to the brain and activate the patient's immune system to clear beta-amyloid protein.

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Scientists have long been looking for ways to tackle these plaques, and they discovered one of the most promising ways to fight it is to “tag” the beta-amyloid proteins with antibodies that signal the immune system to attack and destroy them, before they can form plaques.

In the latest study, Mr. Aebischer of the Brain Mind Institute at EPFL and colleagues note that such a treatment needs to be administered in the early stages of memory loss in order to be most effective. The procedure requires repeat injections, which could have adverse effects.

They say their new implantable capsule could offer a safer and highly effectual alternative.

The capsule, described as a "macroencapsulation device," is made of two permeable membranes sealed together with a polypropylene frame. The device is 27 mm in length, 12 mm wide and 1.2 mm thick. It comprises cells taken from genetically engineered muscle tissue that can produce high levels of antibodies that are able to recognize and target beta-amyloid proteins in the brain.

The cells inside the capsule are made not only to be able to produce antibodies, but also to be compatible with patient, in order to not trigger the immune system against them, like a transplant can. This is where the capsule’s membranes come into play. The permeable membranes of the capsules allow the cells to soak up all the nutrients and molecules they need from surrounding tissue.

When the capsule is implantedin tissue under the skin, it gradually releases the antibodies into the bloodstream. The antibodies then travel from blood to the brain to track down and tag beta-amyloid

The device was successfully tested on mice which showed great success. The mice used were a genetic line of mice that is commonly used to replicate Alzheimer’s disease. The test showed substantial reduction of amyloid-β plaque load.

Verily, over a period of 39 weeks, the capsules produced a constant flow of antibodies, which prevented the formation of amyloid-β plaques in the brain. The treatment also decreased the amount of phosphorylation of the protein tau seen in mice. Tau protein is also believed to play a role in Alzheimer's development by forming "tangles" – another hallmark of the disease.

The proof-of-concept study has been hailed as a landmark. The researchers say it clearly demonstrated that implantable capsules can be used safely and successfully to deliver antibodies in treating Alzheimer’s and other neurodegenerative diseases that feature defective proteins.

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Exercise may protect against cognitive decline

A new study conducted by researchers at the University of Miami in Florida, suggests exercise in older age may slow the rate of cognitive decline and knock off a decade of the brain.

Researchers found that adults over the age of 50 who engaged in light or no exercise showed a significantly faster decline in memory and cognitive skills, compared with those who engaged in moderate to intense exercise.

Similar research in the past suggested that any amount of exercise may reduce the risk of Alzheimer's disease by 50%.

Although, these types of studies are in abundance, researchers say it is important to understand how cognitive decline may be slowed by lifestyle factors, especially with an ageing population.

Dr.Clinton B. Wright, of the University of Miami in Florida notes:

"The number of people over the age of 65 in the United States is on the rise, meaning the public health burden of thinking and memory problems will likely grow.”

"Our study showed that for older people, getting regular exercise may be protective, helping them keep their cognitive abilities longer."

For the study, the researchers evaluated data of 876 adults aged 50 and older - an average age of 71 - free of memory and thinking problems that were part of the Northern Manhattan Study.

Participants were asked how often they had exercised in the previous 2 weeks and how long they had exercised for.

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Almost 90% of the participants said they engaged in either light exercise or no exercise at all. The other 10% reported engaging in moderate to high-intensity exercise, such as running, aerobics or calisthenics.

Approximately seven years later, participants had to take part in memory and thinking tests and undergo brain imaging with Magnetic Resonance Imaging (MRI). The same cognitive tests were completed again five years later.

Participants who engaged in light or no exercise demonstrated a decline in memory and thinking skills compared with participants who did moderate or high-intensity exercise over a 5-year period. Researchers said the difference was comparable to 10 years of ageing.

According to the research team, this association remained after accounting for a number of potentially confounding factors, including alcohol consumption, smoking, body mass index (BMI) and blood pressure.

Dr. Wright said:

"Physical activity is an attractive option to reduce the burden of cognitive impairment in public health because it is low cost and doesn't interfere with medications.

Our results suggest that moderate to intense exercise may help older people delay aging of the brain, but more research from randomized clinical trials comparing exercise programs to more sedentary activity is needed to confirm these results."

The study was published online in the journal Neurology.

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