DO YOU HAVE MILD COGNITIVE IMPAIRMENT?

Mild cognitive impairment (MCI) falls somewhere between age-associated memory impairment and early dementia. People with mild cognitive impairment are more forgetful than normal for their age, but they don’t experience other cognitive problems associated with dementia, such as disorientation or confusion about routine activities. Routine tasks such as paying bills, shopping and meal preparation may become challenging but can still be performed. People with MCI may take more time doing these activities and they may make more mistakes. They are generally able to live independently but may be less active socially.

About one in five older adults has some type of MCI. In a 2010 study of nearly 2,000 people, about 16 percent of dementia-free people over age 70 were suffering from MCI. Men were more likely to suffer than women, although women may simply experience dementia at a later age. In the study, risk factors included being a carrier of the APOE ε4 gene (a known risk factor for late-onset Alzheimer’s disease), never having married and having less than nine years of education. In a 2011 study of nearly 1,300 women age 85 and older, 23 percent were diagnosed with MCI. The researchers recommend that women this age should be screened for cognitive problems.

The National Institute on Aging/Alzheimer’s Association workgroup has come up with new diagnostic guidelines for MCI due to Alzheimer’s disease. With MCI, people experience gradual cognitive decline due to Alzheimer’s-related brain changes. A person is thought to suffer from MCI if he or she meets the following criteria:

• A friend, family member, doctor or the person in question is concerned about a change in his or her cognition compared to the previous level.

• The person is experiencing more difficulties in one or more cognitive areas such as memory, attention and language than would be expected for his or her age or educational background. Difficulty learning and retaining new information is most common in MCI patients who develop Alzheimer’s-related dementia.

• The person is having trouble performing complex tasks such as paying bills, preparing a meal or shopping. He or she may take more time, be less efficient and make more mistakes than in the past. Still, he or she maintains his or her independence with minimal assistance.

• There’s no evidence of significant impairment in social or occupational functioning.

• There should be objective evidence of progressive cognitive decline over time. Cognitive testing can assess the degree of impairment. Scores for people with MCI are usually 1 to 1.5 standard deviations below the mean for their age and education level. Some formal cognitive tests that assess both immediate and delayed recall can help identify MCI patients who are likely to progress to Alzheimer’s dementia within a few years. Other tests can determine impairment in problem-solving, reasoning and language. Doctors may also assess a person’s cognitive function using informal techniques, like asking a patient to learn a street address and then remember it after a delay.

• Vascular, traumatic and medical illnesses that could explain the decline in cognition must be ruled out. The goal is to increase the likelihood that the underlying cause of MCI is probably Alzheimer’s.

• If a person is known to carry a genetic defect, such as a mutation in APP, PS-1 or PS-2, he or she most likely has MCI due to Alzheimer’s disease. Most of these carriers develop Alzheimer’s before age 65. A person who meets the diagnostic criteria for MCI and carries a variant of the Apolipoprotein E (APOE) gene is more likely to progress to Alzheimer’s dementia within a few years than someone without it.

Researchers have discovered that activities such as exercise and computer use may prevent MCI. In a 2010 Mayo Clinic study, adults between ages 70 and 90 who participated in moderate physical exercise like brisk walking or biking and used a computer were less likely to develop MCI. Another Mayo Clinic study found that consuming more heart-healthy mono- and polyunsaturated fats reduced the risk of MCI among people age 70 and older. These fatty acids—which are found in olive oil, nuts, seafood and vegetable oils—appear to prevent inflammation and reduce the risk of blood clots, stroke and heart disease.

Many experts believe that MCI may be an early warning sign of memory disorders later in life. Studies show that up to 15 percent of people with MCI progress to Alzheimer’s disease each year, compared with a rate of 1 to 2 percent a year for the general older population.

(Source:  Health After 50, 14 April 2016)

4 MEMORY SYSTEMS OF THE BRAIN AND DEMENTIA

Normal aging leads to changes in the brain, especially in areas involved in learning and memory.

Over time, changes in the brain can make it more difficult for an older person to learn new tasks or to retrieve information from memory, such as someone's name.

With Alzheimer's disease or a related dementia, the damage is more severe and ultimately affects larger regions of the brain.

The human brain contains an estimated 100 billion nerve cells (neurons). Chemical and electrical activity allows these neurons to perform their tasks and to communicate with one another. This elaborate communication system controls vital body functions and enables us to think, see, move, talk, remember, and experience emotions.

There are four different memory systems of the brain -- episodic, semantic, procedural, and working.

Memory Systems

Episodic Memory

The temporal lobe, which contains the hippocampus, and the prefrontal cortex are important to episodic memory, which enables us to learn new information and remember recent events. The hippocampus is one of the first brain structures damaged in Alzheimer's disease and accounts for one hallmark of early Alzheimer's: difficulty remembering recent events, without any trouble remembering events from long ago.

Semantic Memory

Semantic memory governs general knowledge and facts, including the ability to recognize, name, and categorize objects. This system also involves the temporal lobes and, researchers suspect, multiple areas within the cortex. People with Alzheimer's disease may be unable to name a common object or to list objects in a category, such as farm animals or types of birds.

Procedural Memory

The cerebellum is one of the structures involved in procedural memory. Procedural memory is what enables people to learn skills that will then become automatic (unconscious), such as typing or skiing. This memory system typically is not damaged in Alzheimer's disease or is one of the last cognitive domains to deteriorate.

Working Memory

Working memory involves primarily the prefrontal cortex. This memory system governs attention, concentration, and the short-term retention of needed information, such as a street address or phone number. Problems with working memory can impair a person's ability to pay attention or to accomplish multi-step tasks. Numerous cognitive disorders, such as Alzheimer's, Parkinson's, and Huntington's disease as well as dementia with Lewy bodies, can affect working memory.

In a nutshell, persons living with Alzheimer's or dementia cannot remember to remember. As a result, they can no longer either recall or use new memories in the future.

Nevertheless, persons living with dementia continue to surprise us with their stories and memories of the past.

This should be the focus of our compassionate caregiver efforts.

(Sources of information: John Hopkins +Alzheimer's Reading Room)

ADVICE TO HELP YOU IMPROVE OVERALL MEMORY

Although memory impairment is common as we age and usually is not a sign of a serious neurological disorder, it can be frustrating and socially embarrassing. The minor memory lapses that occur with age-associated memory impairment can't be eliminated completely; however, a number of strategies can improve overall memory at any age.

Place commonly lost items in a designated spot. If you're prone to losing certain items, such as keys or eyeglasses, pick a spot and always put the items there when you are not using them.

Write things down.  If you have trouble remembering phone numbers or appointments, write them down and place the list in a conspicuous spot. Making a daily "to do" list will remind you of important tasks and obligations.

Say words out loud.  Saying "I've turned off the stove" after doing so will give you an extra verbal reminder when you later try to recall whether the stove is still on.

Use memory aids.  Use a pocket notepad, cell phone, wristwatch alarm, voice recorder or other aids to help remember what you need to do or to keep track of information.

Use visual images.  When learning new information, such as a person's name, create a visual image in your mind to make the information more vivid and, therefore, more memorable.

Group items using mnemonics.  A mnemonic is any technique used to help you remember. For example, when memorizing lists, names, addresses and so on, try alphabetizing them or grouping them as an acronym -- a word made from the first letters of a series of words (for example, NATO stands for North Atlantic Treaty Organization).

Concentrate and relax. To remember something, concentrate on the items to be remembered. Pay close attention to new information and try to avoid or block out distractions. It is also beneficial to relax.

Get plenty of sleep. During sleep the brain consolidates and firms up newly acquired information. Studies indicate that people are better at remembering recently learned information the next day if they have had a good night's sleep.

Rule out other causes of memory loss. If you suspect that you are having memory difficulties, consult your doctor. Some medical conditions and certain other factors can cause memory problems that can be corrected. These include depression, hearing or vision loss, thyroid dysfunction, certain medications, vitamin deficiencies and stress.

(Source:  Scientific American Health After 50 Alerts, 16 February 2015)

DEMENTIA AFFECTS "TASTE" MEMORY: DID YOU KNOW?

Getting enough to eat is a fairly common challenge for people with dementia. A study from Japan suggests that trouble recognizing familiar foods or remembering what a dish tastes like could play a role.

The investigators recruited 65 older adults: 30 had Alzheimer's disease, 20 had vascular dementia and 15 healthy participants served as controls. The participants were presented with replicas (so there would be no odors) of three popular dishes in Japan. They were asked to name the dishes and then to identify replicas of food materials included in them. Participants were also asked to name and describe expected tastes -- such as "sweet," "salty" or "bitter" -- of 12 replica foods.

What they found. Compared with healthy controls, those with Alzheimer's disease and vascular dementia had significantly lower scores on the food and taste cognition tests. Eight of 12 dementia patients, described as poor eaters, had especially low taste cognition scores. Imaging studies showed that taste cognition disorders in those with dementia were highly related to damage of the insular cortex -- a region of the brain associated with taste.

If your loved one is not eating enough, talk to the doctor. Any number of problems could be responsible; for example, difficulty swallowing. If a medical cause is ruled out, support groups or Alzheimer's disease organizations can be good sources for practical ways to deal with mealtime challenges.

This study was published in International Psychogeriatrics (Volume 26, page 1127).

(Source:  Scientific American Health After 50 Alerts, 26 February 2015)

TO KEEP YOUR MIND SHARP: DON’T SKIMP ON SLEEP

The health benefits of a proper night's rest have been shown to help numerous conditions, from hypertension to diabetes and depression. Now, increasing evidence points to the importance of good-quality sleep in keeping your memory and cognitive abilities sharp, too.

Experts recommend that older adults get seven to eight hours of sleep each night for overall good health and optimal functioning. Unfortunately, that may be easier said than done because sleep patterns change with age, and older individuals report more problems in getting to -- and staying -- asleep.

According to the National Institute of Health that nearly half of people aged 60 or older report insomnia. In addition, their sleep is not as deep as it was at a younger age, and they tend to wake more often during the night. Chronic pain, increased sensitivity to noise, and medical problems like obstructive sleep apnea and restless legs syndrome also rob older individuals of restorative sleep.

Sleeping Pill Precautions

Be aware that sleeping pills can affect your memory and cognitive abilities. This is particularly true with benzodiazepine-type sedatives, such as diazepam (Valium), temazepam (Restoril), lorazepam (Ativan), oxazepam (Serax) and alprazolam (Xanax and others). Medications in this class have been shown to increase the risk of cognitive impairment and delirium in older adults. Consequently, the American Geriatrics Society (AGS) recommends that drugs in this class not be used for the treatment of insomnia in seniors.

In addition, short-term memory loss has been linked to the over-the-counter antihistamine diphenhydramine (Benadryl), which is also an ingredient in sleep aids such as Tylenol PM and Unisom.

Newer sleep medications, including zolpidem (Ambien and others), eszopiclone (Lunesta) and ramelteon (Rozerem), have come under scrutiny because of reports that some people have experienced incidents like walking, eating or even driving while sleeping during the first few hours after taking the medication, yet having no memory of it the next day. As a further precaution, the FDA warns people who take zolpidem extended-release (Ambien CR) -- either 6.25 mg or 12.5 mg -- not to drive or engage in other activities that require complete mental alertness the following day because levels of the drug can remain high enough to impair these activities.

(Source:  Scientific American Health After 50 Alerts, 2 March 2015)

MEMORY LOSS: IT’S NOT INEVITABLE

The brain contains about 100 billion neurons. A common misconception is that tens of thousands of neurons die each day. In reality, few neurons die over a person's lifetime, but they do shrink. This shrinkage may partially explain why mental functioning slows in middle and older age. (Serious memory problems do occur when major disorders such as a stroke or Alzheimer's destroy whole clusters of neurons.)

In addition to the shrinkage of neurons, starting in middle age the brain begins producing smaller quantities of many neurotransmitters -- chemical messengers that relay information between nerve cells. Brain blood flow is also reduced 15 to 20 percent between ages 30 and 70, although the shrinkage of neurons may account for the reduced flow because less tissue requires less blood.

Cultural attitudes and preconceptions about aging and memory loss can also influence the occurrence of memory lapses as people age. In one study, researchers compared the memory skills of two groups known to harbor few stereotypes concerning old age -- the people of China and deaf Americans -- with those of a third group known to have numerous preconceptions about aging, hearing Americans. Among these preconceptions is the notion that aging causes an inevitable decline in memory skills.

The study results suggest that there is a strong link between culture and memory: The first two groups were less forgetful than the third group, and older Chinese participants performed as well as the younger people in each of these groups. The implication is that if people expect their memory to get worse, they may be less diligent in trying to remember.

Other research indicates that the mental processes required to remember newly acquired information are the same as those needed to retrieve memories from long ago -- something most older people do quite well. This finding implies that older people retain the capacity to recall recent events, but the new information is not being recognized as important or is being discarded instead of stored.

Some researchers interpret this to mean that occasional memory lapses may result from a failure to pay close attention to the information rather than an inability to remember. Thus, it appears that forging new memories depends in large part on staying interested, active and alert.

(Source:  John Hopkins Health Alert, 14 July 2014)

CONCUSSIONS MAY LEAD TO ALZHEIMER'S PLAQUE BUILDUP FOR SOME

Concussions have already been linked to the Alzheimer’s-like degenerative brain disease chronic traumatic encephalopathy (CTE) in athletes and military members who have experienced repeated head blows and traumatic brain injuries.

Now, a new study links concussions to Alzheimer’s disease itself.

Mayo Clinic researchers gave brain scans to 141 Minnesotans who had been experiencing memory problems, and found those who had suffered a brain injury that caused them to black-out had more amyloid plaques in their brain than those who hadn’t.

Amyloid plaque is the telltale sign of Alzheimer’s disease, formed by pieces of a sticky protein that break off in the brain and clump together. Some clumps may form in brain regions involved in learning, memory and thinking, the Alzheimer’s Association explains. More plaques form as the disease progresses.

Researchers gave brain scans to 448 people without any memory or cognitive problems, and 141 people who had mild cognitive impairment (MCI), a condition characterized by declines in memory and thinking skills that aren’t caused by aging. They were also asked whether they had ever experienced a brain injury that caused them to lose consciousness. People with MCI are at a heightened risk of developing Alzheimer’s or another type of dementia, but not everyone with the condition will get worse.

The researchers found 18 percent of those with MCI had reported a prior brain injury, and on scans, they saw the patients had an average of  18 percent more amyloid plaques than those with no history of head trauma. They found no plaque differences in any of the brain scans of people without memory problems, regardless of whether they'd had a brain injury.

"Interestingly, in people with a history of concussion, a difference in the amount of brain plaques was found only in those with memory and thinking problems, not in those who were cognitively normal," study author Dr. Michelle Mielke, a researcher who studies the epidemiology of neurodegenerative diseases at the Mayo Clinic in Rochester, Minn, said in a statement. “The fact that we did not find a relationship in those without memory and thinking problems suggests that any association between head trauma and amyloid is complex."

The study was published on 26 December 2013 in Neurology.

One expert not involved in the study thinks the research may lead to earlier interventions to protect injured brains.

"Drugs that block the development of amyloid or increase its removal from the brain may help protect persons with traumatic brain injury from Alzheimer's disease, though that has not been demonstrated," Dr. Richard Lipton, Director of the Division of Cognitive Aging and Dementia and the Montefiore Headache Center at Albert Einstein College Of Medicine in New York City, told USA Today.

In October, a study found seniors who reported poor quality sleep were more likely to accumulate amyloid plaques in the brain than those who got more than five hours of shut-eye each night.

(Source:  CBS News, 27 December 2013)

WHERE ALZHEIMER'S STARTS, WHY IT STARTS THERE, AND HOW IT SPREADS THROUGHOUT THE BRAIN

Alzheimer’s disease starts in the entorhinal cortex (yellow).

Using fMRI in mouse (left) and human (right) brains, the researchers provide evidence that the disease spreads from the entohrinal cortex (yellow) to other cortical regions (red) — the perirhinal cortex and posterior parietal cortex.

Study Shows Where Alzheimer’s Starts and How It Spreads

Using high-resolution functional MRI (fMRI) imaging in patients with Alzheimer’s disease and in mouse models of the disease, Columbia University Medical Center (CUMC) Researchers have clarified three fundamental issues about Alzheimer’s:

·                     where it starts,

·                     why it starts there,

·                     and how it spreads.

In addition to advancing understanding of Alzheimer’s, the findings could improve early detection of the disease, when drugs may be most effective. The study was published today in the online edition of the journal Nature Neuroscience.

“It has been known for years that Alzheimer’s starts in a brain region known as the entorhinal cortex,” said Co-Senior Author Scott A. Small, MD, Boris and Rose Katz Professor of Neurology, Professor of radiology, and Director of the Alzheimer’s Disease Research Center. “But this study is the first to show in living patients that it begins specifically in the lateral entorhinal cortex, or LEC. The LEC is considered to be a gateway to the hippocampus, which plays a key role in the consolidation of long term memory, among other functions. If the LEC is affected, other aspects of the hippocampus will also be affected.”

The study also shows that, over time, Alzheimer’s spreads from the LEC directly to other areas of the cerebral cortex, in particular, the parietal cortex, a brain region involved in various functions, including spatial orientation and navigation. The researchers suspect that Alzheimer’s spreads “functionally,” that is, by compromising the function of neurons in the LEC, which then compromises the integrity of neurons in adjoining areas.

A third major finding of the study is that LEC dysfunction occurs when changes in tau and amyloid precursor protein (APP) co-exist.

“The LEC is especially vulnerable to Alzheimer’s because it normally accumulates tau, which sensitizes the LEC to the accumulation of APP. Together, these two proteins damage neurons in the LEC, setting the stage for Alzheimer’s,” said Co-Senior Author, Karen E. Duff, PhD, Professor of Pathology and Cell Biology (in psychiatry and in the Taub Institute for Research on Alzheimer’s Disease and the Aging Brain) at CUMC and at the New York State Psychiatric Institute.

In the study, the researchers used a high-resolution variant of fMRI to map metabolic defects in the brains of 96 adults enrolled in the Washington Heights-Inwood Columbia Aging Project (WHICAP).  All of the adults were free of dementia at the time of enrollment.

“Dr. Richard Mayeux’s WHICAP study enables us to follow a large group of healthy elderly individuals, some of whom have gone on to develop Alzheimer’s disease,” said Dr. Small. “This study has given us a unique opportunity to image and characterize patients with Alzheimer’s in its earliest, preclinical stage.”

The 96 adults were followed for an average of 3.5 years, at which time 12 individuals were found to have progressed to mild Alzheimer’s disease.  An analysis of the baseline fMRI images of those 12 individuals found significant decreases in cerebral blood volume (CBV) — a measure of metabolic activity — in the LEC compared with that of the 84 adults who were free of dementia.

A second part of the study addressed the role of tau and APP in LEC dysfunction. While previous studies have suggested that entorhinal cortex dysfunction is associated with both tau and APP abnormalities, it was not known how these proteins interact to drive this dysfunction, particularly in preclinical Alzheimer’s.

To answer this question, explained first author Usman Khan, an MD-PhD student based in Dr. Small’s lab, the team created three mouse models, one with elevated levels of tau in the LEC, one with elevated levels of APP, and one with elevated levels of both proteins. The researchers found that the LEC dysfunction occurred only in the mice with both tau and APP.

The study has implications for both research and treatment.

“Now that we’ve pinpointed where Alzheimer’s starts, and shown that those changes are observable using fMRI, we may be able to detect Alzheimer’s at its earliest preclinical stage, when the disease might be more treatable and before it spreads to other brain regions,” said Dr. Small.

In addition, say the researchers, the new imaging method could be used to assess the efficacy of promising Alzheimer’s drugs during the disease’s early stages.

(Source:  Alzheimer’s Reading Room, 28 December 2013)

DIAGNOSING DEMENTIA: ALZHEIMER'S MAY REALLY BE MINI-STROKES

What causes memory problems? Often, it's plaque in the brain, which leads to Alzheimer's. Now, new research shows a more common culprit may be vascular brain injury. Find out about this type of cognitive decline from stroke, mini-stroke and high blood pressure. Learn why diagnosing the right cause effects therapy and treatment.

Alzheimer's is connected to sticky plaques made of beta-amyloid that choke brain cells, thereby causing dementia. People may act like they have Alzheimer's when they really have vascular dementia. Vascular dementia is caused by vascular events (related to blood vessels) such as strokes and mini-strokes, so treatment is different. (Mini-strokes occur in the brain when blood vessels clog up or burst. They can accumulate slowly and can go unnoticed for years.)

For example, the damage caused by plaque is typically treated with acetylcholinesterase inhibitors like Aricept®. These drugs target the nervous system. Vascular problems like mini-strokes are treated with blood-targeting medications and therapies.

Alzheimer's disease and vascular dementia are two types of dementia that are common in the elderly. A person's dementia can even be caused by a combination of the two, called "Mixed Dementia."

With today's technology, both vascular brain injury as well as beta-amyloid plaque can be detected in the brain. They both cause memory and thinking problems, called "cognitive impairment". If the cognitive impairment is strong and interferes with a typical person's day, it is called dementia. If it is mild, it is called MCI (Mild Cognitive Impairment).

Until now, doctors generally assumed that when they saw cognitive impairment, it was probably from plaque building up in the brain. Treatment and therapy were given accordingly. New research is showing that vascular brain injury from strokes or the mini-strokes often caused by high blood pressure may deserve the greater part of their attention.

A study at the Alzheimer’s Disease Research Center at UC Davis has found that vascular brain injury from conditions such as high blood pressure and stroke are greater risk factors for cognitive impairment among non-demented older people than is the deposition of the amyloid plaques in the brain that long have been implicated in conditions such as Alzheimer’s disease.

Published online early today in JAMA Neurology (formerly Archives of Neurology), the study found that vascular brain injury had by far the greatest influence across a range of cognitive domains, including higher-level thinking and the forgetfulness of mild cognitive decline.

The researchers also sought to determine whether there was a correlation between vascular brain injury and the deposition of beta amyloid (Αβ) plaques, thought to be an early and important marker of Alzheimer’s disease, said Bruce Reed, associate director of the UC Davis Alzheimer’s Disease Research Center in Martinez, Calif. They also sought to decipher what effect each has on memory and executive functioning.

“We looked at two questions,” said Reed, professor in the Department of Neurology at UC Davis. “The first question was whether those two pathologies correlate to each other, and the simple answer is ‘no.’ Earlier research, conducted in animals, has suggested that having a stroke causes more beta amyloid deposition in the brain. If that were the case, people who had more vascular brain injury should have higher levels of beta amyloid. We found no evidence to support that.”

"The second,” Reed continued, “was whether higher levels of cerebrovascular disease or amyloid plaques have a greater impact on cognitive function in older, non-demented adults. Half of the study participants had abnormal levels of beta amyloid and half vascular brain injury, or infarcts. It was really very clear that the amyloid had very little effect, but the vascular brain injury had distinctly negative effects.”

“The more vascular brain injury the participants had, the worse their memory and the worse their executive function – their ability to organize and problem solve,” Reed said.

The research was conducted in 61 male and female study participants who ranged in age from 65 to 90 years old, with an average age of 78. Thirty of the participants were clinically “normal,” 24 were cognitively impaired and seven were diagnosed with dementia, based on cognitive testing. The participants had been recruited from Northern California between 2007 to 2012.

The study participants underwent magnetic resonance imaging (MRI) ― to measure vascular brain injury ― and positron emission tomography (PET) scans to measure beta amyloid deposition: markers of the two most common pathologies that affect the aging brain. Vascular brain injury appears as brain infarcts and “white matter hyperintensities” in MRI scans, areas of the brain that appear bright white.

The study found that both memory and executive function correlated negatively with brain infarcts, especially infarcts in cortical and sub-cortical gray matter. Although infarcts were common in this group, the infarcts varied greatly in size and location, and many had been clinically silent. The level of amyloid in the brain did not correlate with either changes in memory or executive function, and there was no evidence that amyloid interacted with infarcts to impair thinking.

Reed said the study is important because there’s an enormous amount of interest in detecting Alzheimer’s disease at its earliest point, before an individual exhibits clinical symptoms. It’s possible to conduct a brain scan and detect beta amyloid in the brain, and that is a very new development, he said.

“The use of this diagnostic tool will become reasonably widely available within the next couple of years, so doctors will be able to detect whether an older person has abnormal levels of beta amyloid in the brain. So it’s very important to understand the meaning of a finding of beta amyloid deposition,” Reed said.

“What this study says is that doctors should think about this in a little more complicated way. They should not forget about cerebrovascular disease, which is also very common in this age group and could also cause cognitive problems. Even if a person has amyloid plaques, those plaques may not be the cause of their mild cognitive symptoms.”

(Source:  Alzheimer’s and Dementia Weekly, 11 December 2013)

HOW HYPERTENSION AFFECTS MEMORY

Two out of three Americans age 60 and older have some form of high blood pressure -  which is blood pressure that measures 140/90 mm Hg or higher. Hypertension (the medical term for high blood pressure) affects Americans from all walks of life. Yet even though high blood pressure is easy to detect and is almost always treatable, too few people know that they have high blood pressure or even know much about it.

How does high blood pressure impact memory? The most obvious way is via stroke, which occurs when an artery supplying blood to a portion of the brain becomes blocked or suddenly ruptures.

Each year approximately 700,000 Americans suffer strokes, and many die because of them. Of those 500,000 who survive their first stroke, about 25 percent will have a second stroke within five years.

The damage to brain cells caused by a stroke can produce lasting disabilities that may impair a person's memory, senses, motor skills, behavior, language ability and thought processes. The specific deficits that occur depend on which portions of the brain are damaged, as well as the type and severity of the stroke.

Hypertension is a major risk factor for stroke. High blood pressure damages blood vessels that carry blood to the brain, and this damage leads to the buildup of arterial plaque, an accumulation of inflammatory cells, cholesterol and other tissue products within blood vessels. When one of these plaques ruptures, it travels through an artery and eventually gets lodged in a place where the diameter of the plaque is larger than the diameter of the blood vessels. This causes a blood clot to form at that spot.

If the clot completely cuts off blood supply to brain cells responsible for memory or other cognitive functions, the cells die. The death of these cells then leads to impairments in thinking, moving and sensing.

Having high blood pressure is also linked with greater declines in cognitive function when a stroke occurs. In a prospective, observational study, investigators tracked stroke incidence and cognitive performance among 9,704 women ages 65 and older. They found that among participants who had suffered strokes, those who had normal blood pressure before the stroke had better cognitive function afterward than those who were hypertensive beforehand.

(Source:  John Hopkins Health Alert,16 December 2013)

TO DRINK OR NOT TO DRINK: ALCOHOL AND MEMORY

Alcohol's effects on memory depend on the amount consumed. Heavy alcohol consumption, especially binge drinking, takes a toll on memory function. In a study published in epidemiology, midlife binge drinking more than tripled the risk of developing dementia in later life. (Binge drinking was defined as consuming more than five bottles of beer or one bottle of wine on one occasion at least monthly.) The risk of dementia was more than 10 times higher among drinkers who had passed out at least twice during one year.

In contrast, mild to moderate drinking appears to have a protective effect on memory. The source of this protection is not fully understood, but modest alcohol consumption is believed to improve blood flow in the brain and may help prevent small "silent" strokes.

In research published in the Journal of the American Medical Association, investigators reported that people who drank one to six alcoholic beverages a week had a 54 percent lower risk of dementia than people who never drank. Consuming 14 or more drinks per week, in contrast, was associated with an increased risk of dementia.

Some research shows that being a nonsmoker factors into the protective effect of alcohol. A study published in the Journal of Alzheimer's Disease found that those who consumed a moderate amount of alcohol had a lower risk of developing Alzheimer's - especially if they were nonsmokers.

Although no optimal level of alcohol consumption has been established, experts recommend that men consume no more than two drinks per day and women, no more than one drink per day. (One drink equals 12 oz. of regular beer, about 5 oz. of wine or 1.5 oz. of 80-proof distilled liquor.) Women who have an elevated risk of breast cancer should talk with their doctors about drinking alcohol, because as little as one drink a day can boost breast cancer risk. Research is still emerging on how the type of alcohol -  beer, wine or liquor - affects dementia risk.

Despite the apparent cognitive benefits of moderate alcohol consumption, nondrinkers should not start drinking to prevent dementia. The risks of excessive alcohol consumption are many, including alcoholism and automobile accidents.

(Source:  John Hopkins Health Alert, Memory, posted 4 November 2013)

HOW WE MAKE MEMORIES

The human brain contains an estimated 100 billion nerve cells (neurons). All memories are the result of signals that pass through those neurons. But normal aging leads to changes in the brain. Some neurons shrink; others are disabled by damaging molecules called free radicals. Areas of the brain involving memory and learning are particularly affected. Over time, these changes can make it more difficult for an older person to learn new tasks or to retrieve information from memory, such as someone's name. With Alzheimer's disease, the damage is more severe and ultimately affects larger regions of the brain.

The way in which the information that we see, hear and learn each moment is stored in our brains and then made available to be recalled is a complex process. While new theories are still being proposed, the most widely held model proposes that memories are formed in three stages:

Stage 1 : Memory Acquisition

Learning new information activates neurons (nerve cells) in the brain. Communication among these nerve cells encodes the information, creating a temporary neuronal pathway that holds the information as a short-term memory.

If you perceive something visual or spatial, such as a picture, the pathway is created in the right parietal lobe; if you're reading, the pathway forms in the area of the brain that processes language, the left temporal lobe. Focusing attention on new information promotes the encoding process, which then helps it solidify from short- to long-term memory during consolidation. That means that if you have a problem remembering something, maybe you weren't concentrating on it too hard in the first place.

Stage 2 : Memory Consolidation

For information to be retained long term, the neural pathway formed during memory acquisition must be strengthened. The replaying of events in the brain strengthens the pattern of neuronal activity, as more elaborate connections (or synapses) are formed among the neurons.

-  The brain region known as the hippocampus plays a key role in consolidating declarative memories (those related to names, dates, faces, facts and specific events) and is more vulnerable to decline during aging and Alzheimer's disease.

-  Procedural memories, which deal with skills you acquire (like riding a bicycle), are consolidated throughout the frontal lobes, cerebellum and basal ganglia. These memories hold up better over time and can survive even into dementia.

Stage 3 :  Memory Retrieval

In order to recall something, the brain must reactivate the nerve pathways where the specific memory is stored. Frequently retrieved memories are easier to recall, whereas infrequently retrieved information often takes longer to emerge and may require a prompt of some kind, such as a related piece of information.

(Source:  John Hopkins Health Alert, posted 21 October 2013)

COPING WITH A DIAGNOSIS OF EARLY-STAGE DEMENTIA

When you reach age 65, you have a one in 10 chance of developing dementia during your remaining lifetime. Clinicians are now making a concerted effort to diagnose dementia in the early stages, when patients may still have the capacity to understand the disease's course and to make important decisions about future care and interventions.

Being told you have an incurable disease that slowly robs intellectual functioning can take an emotional toll. Adjusting to a diagnosis at any stage of dementia is a complex, evolving process for the person diagnosed and his or her family. You may experience mixed feelings and a range of reactions, including:

A loss of Self

Dementia poses a threat to personality and character. Understandably, dementia's symptoms, such as forgetting faces and struggling to express yourself, can leave feelings of loss, uncertainty and frustration. Experiencing acute grief and mourning your loss of self-identity is common.

Unawareness

Most individuals with Alzheimer's disease aren't aware they have impaired memory and thinking. For others, unawareness increases as the disease progresses. This suggests that unawareness is part of the brain disease in some individuals. Arguing with them or repeatedly demonstrating to them that they're forgetful won't help and is likely to upset them more.

Denial

Other individuals outwardly deny or ignore the diagnosis of dementia but seem to be aware from their behavior that they have a problem. Research suggests that this reaction can sometimes be a self-monitoring strategy in an attempt to be seen by others as a person, not an object, and maintain self-esteem.

Relief

Certain individuals and their loved ones report feeling relief upon hearing the diagnosis of dementia. The anxiety of not knowing what's causing symptoms like forgetfulness can be a tremendous burden. A diagnosis can confirm suspicions that dementia is the cause and legitimizes the need for support and therapeutic interventions.

Secretiveness or Embarrassment

It's common for individuals to be reluctant to reveal their dementia diagnosis for fear of how others might perceive them. As a result, these individuals are often tempted to stop seeing friends or family members and become socially isolated - outcomes that are clearly undesirable, since studies show that maintaining social connectedness is key to coping with the psychological impact of a dementia diagnosis.

Anxiety, Anger, Sadness or Depression

These are all normal reactions. Demoralization is especially common in the disease's early stages the same way it is when grieving any other loss. Behavioral therapy or counseling may ease feelings of anxiety and depression if they interfere with everyday functioning.

(Source:  John Hopkins Health Alert, Posted Memory, 2 September 2013)

RESEARCH ON VASCULAR DEMENTIA AND EXERCISE

Mental decline in older adults who live independently can be delayed if they get regular physical activity, says a new study. Specifically, the study reports that exercise can reduce the risk of vascular-related dementia by more than 50 percent and cognitive impairment without dementia by 60 percent.

Vascular dementia results from blood vessel disease and is associated with conditions like high blood pressure, plaque buildup in artery walls, diabetes and stroke.

The study, which was reported in the online edition of Stroke, followed 638 people, average age of 74, for three years. Sixty-four percent said they were physically active 30 minutes a day for three days a week.

Their activities involved walking, biking and taking gym classes. The results were disappointing, however, when it came to protecting against Alzheimer's. Researchers found no relationship between activity and the risk of developing Alzheimer's. 

(Source:  John Hopkins Health Alert, Memory 22 July 2013)

DETERMINING THE EXTENT OF ALZHEIMER’S DISEASE WITH BRAAK STAGING

Normally, tau protein is used by the brain's neurons as a kind of "scaffolding." But for reasons that are still unclear, as people age the tau protein starts to aggregate into filaments inside the neurons. These tau filaments soon grow out of control, eventually forming distinctive tau tangles. They fill up the neurons and cause them to burst. At this point, neuron death is unstoppable.

Braak staging - developed by German pathologist Heiko Braak - is a way to measure the severity of Alzheimer's disease based on how many tau tangles there are in the brain, and where they are, based on brain autopsy. 

Braak Stage 1 - Braak stage 1 is the point at which tau protein starts to clump into tau tangles. In stage 1 there are no external symptoms and it might take many years before there is noticeable dementia. Nearly everyone will reach Braak stage 1 between 40 and 90 years of age. About 30 percent of 50-year-olds will reach Braak stage 1.

Braak Stage 2 - Tau tangles have accumulated further and have caused some neurons to burst apart and die. Mental testing reveals minimal impairment. Tau tangles at this are found in the brains of about 60 percent of people over age 65. 

Braak Stage 3 - Tau tangles and neuronal death have likely caused some memory impairment, but only about 10 percent of patients will be diagnosed as suffering from dementia. About 45 percent of 80-year-olds have reached this stage. 

Braak Stage 4 - Tau tangles are beginning to form in the outer layers of the cerebral cortex. The patient is experiencing significant impairments in memory and other aspects of cognitive function. 70 percent of patients with this level of tau tangles in the brain will be diagnosed with dementia.

Braak Stage 5 - Tau tangles have caused extensive neuronal death, giving rise to severe memory and cognitive impairment. They are beginning to involve deep areas of the brain that control the initiation of movement. About 80 percent of patients with this level of tangles will be diagnosed with moderate to severe dementia.

Braak Stage 6 - Tau tangles have formed extensively throughout the brain and have caused extensive neuronal death. The outer layers of the brain that integrate activities and the deep areas of the brain that control movement are filled with tau tangles. All patients with this many tau tangles in the brain will be diagnosed as suffering from severe dementia. They will be completely unable to care for themselves and will have difficulty recognizing family members

(Source:  John Hopkins Health Alert, Memory on 29 July 2013)