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.

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

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.

Read More

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.

Read More

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

Read More

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.

Read more Gumdisease may worsen Alzheimer’s symptoms

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.

Read more BellyFat May Cause Cognitive Impairment

"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.

Read More

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.

Read more BellyFat May Cause Cognitive Impairment

“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.

Read more Exercisemay protect against cognitive decline

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.

Read More

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.

Read More

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.

Read more Research shows narcolepsy medication modafinil will actually make you smart

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.

Read More

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.

Read more Just 30 minutes of exercise a day may help relieve asthma symptoms

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.

Read More

Alzheimer’s brain plaques found in people with traumatic brain injury

A new study, published in the journal Neurology suggests people with traumatic brain injury (TBI) may have buildup of plaques similar to those found in the brains of Alzheimer’s patients. Although these amyloid plaques match, their spatial distribution differs.

A corresponding editorial says that over the past decade the rate of emergency department visits related to traumatic brain injury (TBI) has increased by 70% in the United States. The editorial also says an estimated three to five million Americans live with a TBI-related disability.

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

TBI occurs when the brain experiences damage due to a sudden trauma.

Study author Prof. David Sharp, MD, of Imperial College London said:

"The study is small and the findings preliminary; however, we did find an increased buildup of amyloid plaques in people who had previously sustained a traumatic brain injury.”

"The areas of the brain affected by plaques overlapped those areas affected in Alzheimer's disease, but other areas were involved. People after a head injury aremore likely to develop dementia, but it isn't clear why. Our findings suggest TBI leads to the development of the plaques which are a well-known feature of Alzheimer's disease."

People who suffer from TBI can have a slew of medical issues. While some TBI patients may experience cognitive impairments or difficulty with sensory information, others might have display mental health issues such as anxiety or depression. Yet, another long-term risk factor TBI patients is dementia. Scientists do not know the exact mechanism behind this relationship, but recent studies have made some progress into understanding it.

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

For the study, researchers recruited 9 people with an average age of 44 who had a single moderate to severe TBI. Their brain injuries had occurred between 11 months and 17 years previously. The research team took an in-depth look at their brains by taking PET and MRI scans. The PET scans detected amyloid plaques in the brain and the MRI scans searched out evidence of cellular damage resulting from the trauma.

The scan results were compared with 10 people with Alzheimer's disease and nine healthy participants (control group).

Both the people with brain injuries and the people with Alzheimer's disease had plaques in the posterior cingulate cortex, which is affected early in Alzheimer's. The researchers also found that plaques were increased in patients with more damage to the brain's white matter.

Interestingly, the TBI group, but not the Alzheimer's group, also showed plaques in the cerebellum.

Prof. Sharp said:

"It suggests that plaques are triggered by a different mechanism after a traumatic brain injury."

"The areas of the brain affected by plaques overlapped those areas affected in Alzheimer's disease, but other areas were involved.

“It suggests that plaques are triggered by a different mechanism after a traumatic brain injury. The damage to the brain's white matter at the time of the injury may act as a trigger for plaque production."

The current study is a relatively small-scale trial, however, Prof. Sharp believes that if a substantial link can be found between brain injury and the onset of Alzheimer's disease, it might help neurologists uncover treatment and prevention strategies to reduce the progression of Alzheimer's at an earlier stage.

Read More

Growth factor in brain may slow cognitive decline

A new study has found that older people with higher amounts of a key protein from the gene called brain-derived neurotrophic factor, or BDNF in their brains have slower decline in their memory and cognitive skills compared to people with lower amounts of protein from the gene.

People tend to experience decline in physical skills as they age. Although the physical decline is obvious, the brain also has a tendency to slow down.

Read more Blocking brain inflammation stops Alzheimer’s

However, it is not certain that cognitive decline will occur in all older adults. When it does occur, the speed of decline may vary from person to person. Significant impairment can be seen in some individuals, while others may show virtually no change at all.

The reasons behind these neurological differences are mystery to scientists. Since ageing is a multifaceted process and the brain is a complex organ, clues to the causal factors of mental decline with age are difficult to connect.

Dr.Aron S. Buchman and colleagues at the Rush University Medical Center in Chicago, IL, aimed to explore the involvement of BDNF in age-based cognitive decline.

BDNF is a growth factor that encourages the growth of new neurons and synapses, and supports existing neurons. It can be found extensively in both the brain and the peripheral nervous system. Many studies have shown that it is crucial in various important operations, including the maintenance of long-term memories.
Much of the nervous system in mammals is arranged before birth, but parts of the brain retain the ability to grow new neurons in a process called neurogenesis. BDNF is one of the major participants in this creation of new brain substance.

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

The role of BDNF in memory and the protection and development of neurons make it a key candidate for examinations into the cognitive decline seen in many ageing brains.

Rats born without the ability to create BDNF die soon after birth because of neural abnormalities. However, if BDNF is injected into the lateral ventricle of an adult rat, new neurons grow in the striatum, septum, thalamus and hypothalamus.

For the study, researchers recruited 535 people with an average age of 81. These participants were part of the Rush Memory and Aging Project and the Religious Orders Study. They were followed until death, for an average of six years. The participants took yearly tests of their thinking and memory skills, and after death, a neurologist reviewed their records and determined whether they had dementia, some memory and thinking problems called mild cognitive impairment or no thinking and memory problems. Autopsies were conducted on their brains after death, and levels of the gene that codes for BDNF in the brain were measured.

The rate of cognitive decline was about 50% slower for those in the highest 10% of protein from BDNF gene expression compared to the lowest 10%. The effect of plaques and tangles – 2 hallmarks of Alzheimer’s disease –reduced cognitive decline in people with high levels of BDNF. Cognitive decline was about 40% slower for people with the highest amount of protein from BDNF gene expression compared to those with the lowest amount.

On average, thinking and memory skills declined by about 0.10 units per year on the tests. Higher levels of protein from BDNF gene expression reduced the effect of plaques and tangles in the brain on cognitive decline by 0.02 units per year.

The researchers found that the plaques and tangles in the brain accounted for 27% of the variation in cognitive decline, demographics accounted for 3% and BDNF accounted for 2%.

Plaques and tangles can be found in the brains of people with Alzheimer’s. Scientists believe that the plaques and tangles negatively impact cognitive function. The study revealed that the effect of these markers on cognitive decline was reduced by 40% for individuals with the highest levels of BDNF.

Dr. Buchman said:
"This relationship was strongest among the people with the most signs of Alzheimer's disease pathology in their brains.

This suggests that a higher level of protein from BDNF gene expression may provide a buffer, or reserve for the brain and protect it against the effects of the plaques and tangles that form in the brain as a part of Alzheimer's disease."

Buchman noted that the study does not prove that BDNF is the cause of a slower rate of cognitive decline; further work is needed to determine if activities which increase brain BDNF gene expression levels protect or slow the rate of cognitive decline in old age.

The study was published in the online issue of Neurology, the medical journal of the American Academy of Neurology.

Read More

Gum disease may worsen Alzheimer’s symptoms

A new study published in the journal PLOS One suggests there is a link between gum disease and greater rates of cognitive decline in people with early stages of Alzheimer's disease.

Periodontitis or gum disease is an unpleasant condition, causing bad breath, bleeding and painful gums, ulcers and even tooth loss.

The disease is more common in women than men. Persistent bad breath and red, swollen or bleeding gums are common signs of the condition. Poor oral hygiene, smoking and diabetes are all risk factors for gum disease.

The disease is common in older people and may become more common in Alzheimer's disease because of a reduced ability to take care of oral hygiene as the disease progresses.

Read more Exposureto environmental toxin may increase risk of Alzheimer's

Previous studies have shown that higher levels of antibodies to periodontal bacteria are associated with an increase in levels of inflammatory molecules elsewhere in the body. These inflammatory molecules have been linked to greater rates of cognitive decline in Alzheimer's disease.

For the latest study, first study author Dr. Mark Ide, from the Dental Institute at King's College London in the UK, and colleagues aimed to determine whether periodontitis or gum disease is associated with increased dementia severity and subsequent greater progression of cognitive decline in people with Alzheimer's disease.

The researchers gathered 59 participants withmild to moderate Alzheimer's disease. Their cognitive function was evaluated by taking cognitive tests and their blood sample was taken to measure inflammatory markers in their blood. The majority of participants (52) were followed-up at 6 months when all assessments were repeated.

The results showed that the presence of gum disease at study baseline was not related to participants' cognitive state at that point. However, it did appear to be associated to a six-fold increase in cognitive decline over a six-month follow-up period. Additionally, participants who had gum disease at study baseline showed an increase in blood levels of pro-inflammatory markers over the follow-up period.

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

The authors suggest that gum disease is associated with an increase in cognitive decline in Alzheimer's disease, possibly via mechanisms linked to the body's inflammatory response.

Dr. Ide said:

"A number of studies have shown that having few teeth, possibly as a consequence of earlier gum disease, is associated with a greater risk of developing dementia. We also believe, based on various research findings that the presence of teeth with active gum disease results in higher body-wide levels of the sorts of inflammatory molecules which have also been associated with an elevated risk of other outcomes such as cognitive decline or cardiovascular disease. Research has suggested that effective gum treatment can reduce the levels of these molecules closer to that seen in a healthy state."

Researchers admit that limitations of the study included the small number of participants. They advise that the link between gum disease and cognitive decline should be examined in a larger cohort. They said that the precise mechanisms behind this association are not fully clear and other factors might also play a part in the cognitive decline of participants.

Read More