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Seth Rogen’s Hilarity for Charity Brings Serious Attention to Alzheimer’s

Seth Rogen is best known for his role in slapstick comedies like “Knocked Up” and “Superbad.” But there’s another side to the actor, one that is fighting for Alzheimer’s awareness and raising funding for Alzheimer’s research.Seth Rogen's Hilarity for Charity Brings Serious Attention to Alzheimer's

As Rogen watches his mother-in-law battle with the disease, he is raising funds and awareness through his organization “Hilarity for Charity.” Learn more about the organization and how it is bringing serious attention to Alzheimer’s.

Seth Rogen’s Hilarity for Charity

Hilarity for Charity (HFC) is an organization led by Seth Rogen and his wife, Lauren Miller, to fight Alzheimer’s, the disease that plagues his mother in-law. Using his celebrity status and far reaching platform, Rogen and his team strive to raise Alzheimer’s awareness among the millennial generation.

The organization sponsors an annual event called the Los Angeles Variety Show and since the event began three years ago, HFC has raised over $1.7 million for Alzheimer’s. Past performers include Paul Rudd, Bruno Mars, Tenacious D, Patton Oswalt, Samuel L. Jackson and The Backstreet Boys, to name a few. This year’s event, James Franco’s Bar Mitzvah at the Fourth Annual Variety Show, will be held on October 17, 2015 and features Miley Cyrus.

Last year, HFC expanded their reach by launching HFC U to connect with universities and encourages college organizations to host their own HFC event. The organizations compete with each other and the top fundraiser earns a coveted prize. The most recent prize, awarded to Pi Kappa Alpha and Alpha Chi Omega at the University of Vermont, was a live commentary screening of Superbad with Seth Rogen and Chris Mintz-Plasse. The nationwide program has over 230 schools participating and has raised over $200,000.

Hilarity for Charity Brings Serious Attention to Alzheimer’s

There’s no question that Hilarity for Charity is making a financial impact in the fight against Alzheimer’s. However, it is arguably their impact on social awareness that is making the biggest contribution.

The money raised from HFC goes to care, support and raise awareness and research. Hilarity for Charity awards in-home care grants throughout the Unites States and Canada to allow more people to stay at home longer. As of 2015, HFC has given over 8,000 hours of respite care to Alzheimer’s and dementia caregivers.

Another goral is to “mobilize a new generation of Alzheimer’s advocates while supporting young people who are currently affected by the disease.” To do this, HFC provides support and awareness programs for people under 40 fighting Alzheimer’s. A main component of awareness has been the the release of a feature length film, “This is Alzheimer’s” which documents the stories of three different families navigating their way through the disease.

Finally, HFC supports research efforts through the Alzheimer’s Association’s International Research Grant Program.  Of these grants, HFC has supported grants focused on early onset Alzheimer’s.

To learn more about HFC and to learn how you can become involved in their fundraising and awareness efforts visit: www.hilarityforcharity.org

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Alzheimer’s and Intimacy

While it’s no secret that sexual relationships occur among seniors and even seniors with dementia, the topic still remains extremely taboo. A recent trial brought the subject to national headlines and now caregivers everywhere are faced with the question of consensual sex among aging adults with dementiaAlzheimer's and Intimacy

When is dementia too far advanced for a person to consent to sex? Learn more about how assisted living communities are handling Alzheimer’s and intimacy while protecting the safety of residents.

The Controversy Surrounding Alzheimer’s and Intimacy

Sexual relationships among seniors living in assisted living communities are not uncommon, so why is there such a struggle when it comes to discussing seniors with dementia having sex?

The controversy was recently in national headlines when a 78-year-old man in Iowa was charged with raping his wife, who was living in a nursing home and has Alzheimer’s disease. The staff in the community maintained that his wife, their patient, was no longer able to consent to sex. He was eventually found not guilty of the crime but the trial did bring national awareness to a topic that often feels taboo.

The question remains how senior living communities are handling this confusing and emotionally driven issue.

At Hebrew Home in New York, the community has a written policy to clarify any confusion over the sex life of residents and has for 20 years. Daniel Reingold, CEO of RiverSpring Health, the nonprofit that runs Hebrew Home, acknowledges the sensitivity of the issue stating, “It was controversial in 1995 and it’s controversial today.”

He went on to say, “We knew that there was intimacy occurring, and we considered it to be a civil right and a legal right. We also felt that intimacy was a good thing, that touch is one of the last pleasures we abandon and lose as we age.”

Sensitivity Surrounds Issue in Senior Living Communities

While the policy at Hebrew Home is a step in the right direction, law professor at Albany Law School and bioethics professor at Albany Medical College, Evelyn Tenenbaum, cautions that even with a written policy, staff may have trouble differentiating between a consensual and non-consensual relationship.

“For example, suppose you have a couple and the woman believes that the man she’s seeing is her husband,” says Tenenbaum. “Then she consents to a sexual relationship. Is that really consent if she doesn’t understand who he is and that she’s not married to him?”

According to the American Health Care Association, there is no clear answer to defining a consensual sexual relationship when one or both partners has dementia.

Patricia Bach, a geriatric psychologist began looking for data to help clarify the question and found that little empirical evidence even existed. When she surveyed members of the American Medical Directors Association, she found that only 25-30% had completed formal training regarding intimacy and sexuality in seniors.

As the aging population grows this issue is going to become increasingly pressing. What do you think about defining consensual sex when one or both partners has dementia? Share your thoughts in the comments below. 

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I Am More than My Diagnosis

Tim, diagnosed with Frontotemporal dementia in 2012, living with HIV

Working in information technology and then for many years as a part of a management team, my career was very important to me. At the end of 2009, however, I realized that I was having trouble focusing on my job, and one day after a lunchtime walk, I felt like I had lost sight in one of my eyes. Thinking it was due to stress, I didn’t tell my partner Ron. I explained it away.

In early 2010, I took a work trip to Denver. During that week I had issues typing and communicating. When I met with my boss to discuss the trip, I had trouble speaking. That’s when I decided to see a doctor. “After talking to you, I think you need to go to ER right now,” he said.  I found out that I had had a stroke, and doctors suspected that several mini- strokes had also occurred, which accounted for my vision loss.timblog

Despite having some answers, I didn’t have them all. After returning to work a couple of months later, I was still struggling to do my job, which resulted in my being demoted. In January 2012, I was laid off. Due to all of the anxiety I was experiencing, I started seeing a therapist, who suggested that I make lists of coping strategies, but I never made the connection in my head to actually complete the tasks.

While in therapy, I was also undergoing testing and not sharing the results with Ron. I would come home and say “everything is fine” very nonchalantly. Ron knew everything wasn’t. “Either you are not communicating properly or you are just not telling me something,” he said. From then on Ron accompanied me to my appointments. We learned that the results of the testing indicated that there was a problem, but no conclusive diagnosis. Ron crusaded to find out what was really going on.  Eventually, in 2012, after many tests and much anxiety, I was diagnosed with Frontotemporal dementia (FTD), which is caused by progressive cell degeneration that affects the frontal and temporal lobes of the brain.  

Ron is my everything. He is my advocate, my only support, and my protector. If it wasn’t for him, I probably would not have received a diagnosis. I don’t even realize how many times a day he helps me make decisions. He’s good at subtly guiding me, as I can get very easily lost in a task. He is always looking out for my best interest. Because of FTD, I don’t have a perception of what repercussions exist due to my actions. I can’t even imagine what my life would be if I did not have him here.

Having been HIV positive for 25+ years, I treat the diagnosis of dementia like HIV; it doesn’t define who I am or what I can do. I don’t let the dual diagnosis control my life. I present myself first – work experience, life experience – and eventually my story unfolds. When I introduced myself to Congressman Cory Booker, I said, “Something you might not know about me is that I was diagnosed with dementia in 2012.” It was amazing how his constitution changed. “I wouldn’t have known,” he replied. It changed his whole perspective.

I tell people who I speak with on Peer-to-Peer Outreach Program calls that they have to look at their diagnosis as a new adventure. (Peer-to-Peer Outreach is a program of the Alzheimer’s Association that connects newly-diagnosed individuals with others living with Alzheimer’s and other dementias via telephone in order to share their experiences.) It’s a new challenge in your life. You will find different ways to accomplish tasks and you will find talents that you never had before. I never used to be able to speak in front of people. Because of my diagnosis, I can now give a speech. I still have challenges, I still have anxiety, but I have been able to do things I couldn’t do before as well.

As a care partner, Ron has a thankless job. I don’t always acknowledge what he does for me. Some doctors have suggested that the word dementia not be used in front of me and I appreciate that Ron is so honest with me about the diagnosis. Individuals living with dementia deserve to have advocates. You need someone who will go to battle for you. Ron does that for me.

I was losing direction and I needed to find a new outlet, so Ron encouraged me to get involved with the Alzheimer’s Association. Being an Early-Stage Advisory Group (ESAG) member has allowed me to let people know that their life is not over – that life is what you make of it. If I had a tagline like the women do on the Real Housewives reality shows, mine would be: “Get to know me first. I am more than my diagnosis.”

Ron, Tim’s care partner

I knew something was wrong long before Tim received a diagnosis. As his advocate, I helped coordinate his medical team and began making plans for the future. We went to an elder care lawyer (who was very helpful) and sold our home that we spent 10 years renovating .A lot of people wait too long to plan. The sooner you do that the better.

Dementia happened to Tim much earlier than it does for most. He was hoping to work up to 15 more years, build funds for retirement and travel. We moved from the suburbs to a 55+ community, and we live a very different life here. Tim and I have attended support groups through the Alzheimer’s Association, but I have also found support in our community by connecting with other caregivers. While other community members are older and their experiences more varied, their support is still valuable. Almost all of the people that are involved in support groups and services in the community are much older than us and it’s hard to relate to one another. Prepare yourself, because as a care partner, you have to realize it will only become even more intense.

You have to seek out advice. You have to be realistic. It won’t get any better. You have to take advantage of every moment together and celebrate what you have. Your relationship will change greatly. There are times when it’s difficult, and it’s usually little things that push you over the edge. You get by, but it’s very difficult. It is very hard to see your loved one diminish in front of you. I love Tim, but he isn’t who he used to be. As a care partner, you sometimes feel like you have the weight of the world on your shoulders.

It is a heavy journey and it is a process, but you do what you can do. It’s not all gloom and doom, but it has been difficult reflecting on the past three years. Neither of us have a career anymore. We had to sell our home and settle into a new place. Amongst all that, we were working on getting Tim’s diagnosis. I lost both of my parents and Tim’s brother and father passed away – we’ve had so much happen. But we don’t give up. You have to make the best of your situation. I want other care partners and caregivers to know that they shouldn’t give up their whole identity. You have to do things for yourself. Our situation is what it is. You have to try and take in every moment you have and hold on to what you can.

As a member of the Alzheimer’s Association 2014 National Early-Stage Advisory Group (ESAG), Tim Kaufman raises awareness of the financial impact of the disease and the value of an accurate and early diagnosis. He also addresses the needs of lesbian, gay, bisexual and transgender (LGBT) individuals living with dementia. Tim and his partner Ron live in Southampton, New Jersey.

Diet that mimics fasting may promote longevity and improve healthspan

A new study published in Cell Metabolism suggests following a calorie-restricted diet that mimics fasting for just 5 days a month for 3 months may promote longevity and reduce a number of risk factors for cancer, diabetes and cardiovascular disease.
A woman eating healthy food
Researchers found participants who followed a fasting-mimicking diet experienced a reduction in risk factors linked to aging, cardiovascular disease, diabetes and cancer.

Study co-author Valter D. Longo, of the FIRC Institute of Molecular Oncology in Italy and the University of Southern California, and colleagues say the research demonstrates the first anti-aging, healthspan-promoting intervention that doctors could feasibly recommend for patients.

Previous research from Longo in June last year suggested prolonged fasting – defined as consuming only water for 2-4 days – can “reboot” the human immune system. That is, fasting can help clear out damaged cells and regenerate new ones.

Another study published later that month also found periodic fasting may protect against diabetes among individuals at high risk for the condition.

However, Longo and colleagues note that humans find it psychologically challenging to engage in such extreme dieting, and it can also have adverse health effects – particularly for older individuals.

“These concerns point to the need for dietary interventions that induce prolonged fasting-like effects while minimizing the risk of adverse effects and the burden of complete food restriction,” they note.

Fasting diet promoted cell regeneration, extending lifespan in mice

To address this need, the researchers developed a fasting-mimicking diet (FMD) – a low-protein, low-fat diet high in healthy fats. By activating markers associated with prolonged fasting, such as low glucose levels and high levels of ketone bodies, the diet was able to simulate the effects of fasting.

Firstly, the team tested the diet in middle-aged mice, feeding them the diet for 4 days, twice a month. Mice fed the FMD intervention were compared with mice fed a control diet.

The team found mice fed the FMD intervention had much higher numbers of stem cells, and they experienced regeneration of an array of other cell types, including bone, muscle, liver, brain and immune cells, compared with mice fed the control diet.

In addition, the FMD intervention appeared to extend the lifespan of mice and promote better overall health. They experienced better learning and memory, lower incidence of cancer and inflammatory diseases and fat loss without a reduction in lean body mass, compared with control mice.

Reduction in risk factors for aging, CVD, diabetes and cancer in humans

Next, the team tested a similar FMD intervention in a group of 19 generally healthy people aged 18-70. These participants were required to follow the diet for 5 days a month for 3 months. The diet provided them with between 34-54% of their normal caloric intake, as well as 11-14% proteins, 42-43% carbohydrates and 44-46% fat.

The 19 participants following the FMD intervention were compared with a group of 18 generally healthy aged-matched individuals who continued to follow their normal diet.

Compared with the participants who consumed their standard diet, those who followed the FMD intervention experienced a reduction in risk factors linked to aging, cardiovascular disease (CVD), diabetes and cancer, including lowered blood glucose, reduced markers of inflammation and weight loss.

The team notes that only 5% of FMD participants were disqualified from the study for failing to comply with the dietary regime.

Longo and colleagues say their findings indicate that following an FMD intervention periodically may promote longevity in humans and protect against risk factors for certain diseases. They add:

“Although the clinical results will require confirmation by a larger randomized trial, the effects of FMD cycles on biomarkers/risk factors for aging, cancer, diabetes, and CVD, coupled with the very high compliance to the diet and its safety, indicate that this periodic dietary strategy has high potential to be effective in promoting human healthspan.”

The team says they are now putting the FMD intervention through a rigorous testing process in order to gain approval from the US Food and Drug Administration (FDA) for clinical use. This involves testing the efficacy of the diet in 60-70 participants, before moving to a clinical trial with 500-1,000 participants.

“This is arguably the first non-chronic preclinically and clinically tested anti-aging and healthspan-promoting intervention shown to work and to be very feasible as a doctor or dietitian-supervised intervention,” says Longo.

The researchers stress that because the effects of the FMD intervention are potent, individuals should only follow such a diet under medical supervision.

Written by Honor Whiteman

Stories My Grandfather Told Me

I am sitting at a dinner party in Deauville, France, listening to my grandfather recount stories I’ve heard him tell a thousand times before; times spent with Peter O’Toole in the desert, his love affair with Barbra Streisand and with other leading ladies, past exploits at card tables and racetracks.omar1

But this night is different. The stories are off; rich details normally embedded like fine jewels are missing. The characters are colorless and the anecdotes lack grounding in space and time – they just seem to float out of place and order. Attempts at humor have been replaced by an obvious air of anxiety and frustration brought on by his trying to remember.

He’s just tired, I think to myself. He’s been traveling too much. Pay it no mind.

But then he starts the stories over again, seemingly unaware that he’s just finished recounting them.

Something is wrong.

This was my first indication that my grandfather had Alzheimer’s disease, and in the subsequent years, many clues would follow.

omar2It’s the quintessential irony — creating a life filled with cherished memories and relationships only to lose them.

A World Champion bridge player, an Academy Award nominated actor, a man proficient in seven languages with a higher IQ than anyone I’ll likely ever meet…Alzheimer’s does not discriminate in its victims.

It has been a slow and steady decline made all the more apparent by a lack of forward progress towards finding a cure.

So we must unite.

Throughout the month of June, join me in taking the pledge to “Go Purple” for Alzheimer’s awareness and let’s find purplepledgeomara cure together.

Alzheimer’s is a thief — stealing brilliant minds. This disease must be stopped.

 

About the Author: Omar Sharif, Jr. is an Egyptian actor and spokesperson. An advocate for equal human rights, he is the grandson of legendary Hollywood actor Omar Sharif.

Alzheimer’s risk may be predicted by blood protein

Researchers have discovered a blood protein that could indicate the development of mild cognitive impairment – a condition associated with an increased risk of Alzheimer’s disease and other dementias – long before symptoms present themselves.
Gloved hand holding a test tube filled with blood.
Previous studies have suggested that blood could be a useful source of biomarkers for Alzheimer’s disease.

The study, published in Translational Psychiatry, involved data from over 100 sets of twins – including 55 pairs of identical twins – allowing the researchers to demonstrate that any associations discovered between the blood protein and cognitive decline were independent of age and genetics.

Alzheimer’s disease is an age-associated neurodegenerative disorder and the sixth leading cause of death in the US. According to the Alzheimer’s Association, an estimated 5.3 million Americans of all ages have the condition. At present, no treatments are available to prevent the development of Alzheimer’s disease.

“Although we are still searching for an effective treatment for Alzheimer’s disease, what we do know is that prevention of the disease is likely to be more effective than trying to reverse it,” says lead author Dr. Steven Kiddle, a research fellow at King’s College London (KCL) in the UK.

For a prevention trial to be effective, individuals at risk of the disease are required. Individuals at risk from Alzheimer’s disease can be difficult to identify, however. Although magnetic resonance imaging (MRI) and positron emission tomography (PET) brain scans can show visible signs of symptoms before symptoms are presented, these are expensive and require specialized facilities.

Many researchers are searching for surrogate markers that are relatively inexpensive and noninvasive yet provide enough information to benefit prevention trials, the authors write. For the new study, the team examined more than 1,000 proteins in the blood of 212 subjects (106 pairs of twins) using a protein biomarker discovery tool that measured a wide range of different proteins.

Each subject’s cognitive ability was assessed using a computerized test known to be sensitive for detecting early Alzheimer’s disease-related cognitive changes and the results of these were compared with the protein levels measured each individual’s blood.

Further studies required to confirm protein’s status as a biomarker

The researchers discovered that levels of one particular protein – MAPKAPK5 – was lower in the blood of individuals whose cognitive ability declined significantly over 10 years. MAPKAPK5 levels appeared to be associated with cognitive change in both the context of individuals and within pairs of twins.

It is the first time that MAPKAPK5 has been implicated in the development of Alzheimer’s disease, having previously been studied in the context of cancer and rheumatoid arthritis.

“The next step will be to replicate our finding in an independent study, and to confirm whether or not it is specific for Alzheimer’s disease,” says Dr. Kiddle, “as this could lead to the development of a reliable blood test, which would help clinicians identify suitable people for prevention trials.”

If the team can confirm the protein’s status as a biomarker for modifiable cognitive aging, it would be of huge benefit to other researchers aiming to recruit at-risk asymptomatic individuals into prevention trials.

“We’re very optimistic that our research has the potential to benefit the lives of those who don’t currently have symptoms of Alzheimer’s, but are at risk of developing the disease,” concludes co-author Dr. Claire Steves, geriatrician and senior lecturer in Twin Research at KCL.

Funding for the UK-based study was provided by the Medical Research Council (MRC), the National Institute of Health Research Biomedical Research Centre for Mental Health and the Wellcome Trust.

Recently, Medical News Today reported on a study that found a form of medication taken by patients to prevent transplanted organs from rejecting their new bodies could also protect against the development of Alzheimer’s disease.

Written by James McIntosh

Cheri Taylor, Executive Director, Porterville Adult Day Services

A discussion with Cheri Taylor, Executive Director of the Porterville Adult Day Services. If you live in the South Valley, you have a great resource and we recommend that you contact them and see if they can provide some help. Whether you are a caregiver or simply concerned about a loved one, Cheri and her staff go all out in order to provide respite and relief for all involved. Originally aired on 4/30/14.

New potential cause for Alzheimer’s: Arginine deprivation caused by overconsumption by immune cells

Increasingly, evidence supports the idea that the immune system, which protects our bodies from foreign invaders, plays a part in Alzheimer’s disease. But the exact role of immunity in the disease is still a mystery.

A new Duke University study in mice suggests that in Alzheimer’s disease, certain immune cells that normally protect the brain begin to abnormally consume an important nutrient: arginine. Blocking this process with a small-molecule drug prevented the characteristic brain plaques and memory loss in a mouse model of the disease.

Published April 15 in the Journal of Neuroscience, the new research not only points to a new potential cause of Alzheimer’s but also may eventually lead to a new treatment strategy.

“If indeed arginine consumption is so important to the disease process, maybe we could block it and reverse the disease,” said senior author Carol Colton, professor of neurology at the Duke University School of Medicine, and a member of the Duke Institute for Brain Sciences.

The brains of people with Alzheimer’s disease show two hallmarks — ‘plaques’ and ‘tangles’ — that researchers have puzzled over for some time. Plaques are the build up of sticky proteins called beta amyloid, and tangles are twisted strands of a protein called tau.

In the study, the scientists used a type of mouse, called CVN-AD, that they had created several years ago by swapping out a handful of important genes to make the animal’s immune system more similar to a human’s.

Compared with other mice used in Alzheimer’s research, the CVN-AD mouse has it all: plaques and tangles, behavior changes, and neuron loss.

In addition, the gradual onset of these symptoms in the CVN-AD mouse gave researchers a chance to study its brain over time and to focus on how the disease begins, said the study’s first author Matthew Kan, an MD/PhD student in Colton’s lab.

Looking for immune abnormalities throughout the lifespan of the mice, the group found that most immune system components stayed the same in number, but a type of brain-resident immune cells called microglia that are known first responders to infection begin to divide and change early in the disease.

The microglia express a molecule, CD11c, on their surface. Isolating these cells and analyzing their patterns of gene activity, the scientists found heightened expression of genes associated with suppression of the immune system. They also found dampened expression of genes that work to ramp up the immune system.

“It’s surprising, because [suppression of the immune system is] not what the field has been thinking is happening in AD,” Kan said. Instead, scientists have previously assumed that the brain releases molecules involved in ramping up the immune system, that supposedly damage the brain.

The group did find CD11c microglia and arginase, an enzyme that breaks down arginine, are highly expressed in regions of the brain involved in memory, in the same regions where neurons had died.

Blocking arginase using the small drug difluoromethylornithine (DFMO) before the start of symptoms in the mice, the scientists saw fewer CD11c microglia and plaques develop in their brains. These mice performed better on memory tests.

“All of this suggests to us that if you can block this local process of amino acid deprivation, then you can protect — the mouse, at least — from Alzheimer’s disease,” Kan said.

DFMO is being investigated in human clinical trials to treat some types of cancer, but it hasn’t been tested as a potential therapy for Alzheimer’s. In the new study, Colton’s group administered it before the onset of symptoms; now they are investigating whether DFMO can treat features of Alzheimer’s after they appear.

Does the study suggest that people should eat more arginine or take dietary supplements? The answer is ‘no,’ Colton said, partly because a dense mesh of cells and blood vessels called the blood-brain barrier determines how much arginine will enter the brain. Eating more arginine may not help more get into the sites of the brain that need it. Besides, if the scientists’ theory is correct, then the enzyme arginase, unless it’s blocked, would still break down the arginine.

“We see this study opening the doors to thinking about Alzheimer’s in a completely different way, to break the stalemate of ideas in AD,” Colton said. “The field has been driven by amyloid for the past 15, 20 years and we have to look at other things because we still do not understand the mechanism of disease or how to develop effective therapeutics.”


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The above post is reprinted from materials provided by Duke UniversityNote: Materials may be edited for content and length.

Vascular dementia

Vascular dementia

Vascular dementia is the second most common cause of dementia, after AD. It is caused by brain damage from cerebrovascular or cardiovascular problems – usually strokes. It also may result from genetic diseases, endocarditis (infection of a heart valve), or amyloid angiopathy (a process in which amyloid protein builds up in the brain’s blood vessels, sometimes causing hemorrhagic or “bleeding” strokes). In many cases, it may coexist with AD. The incidence of vascular dementia increases with advancing age and is similar in men and women.

Symptoms of vascular dementia often begin suddenly, frequently after a stroke. Patients may have a history of high blood pressurevascular disease, or previous strokes or heart attacks. Vascular dementia may or may not get worse with time, depending on whether the person has additional strokes. In some cases, symptoms may get better with time. When the disease does get worse, it often progresses in a stepwise manner, with sudden changes in ability. Vascular dementia with brain damage to the mid-brain regions, however, may cause a gradual, progressive cognitive impairment that may look much like AD. Unlike people with AD, people with vascular dementia often maintain their personality and normal levels of emotional responsiveness until the later stages of the disease.

People with vascular dementia frequently wander at night and often have other problems commonly found in people who have had a stroke, including depression and incontinence.

There are several types of vascular dementia, which vary slightly in their causes and symptoms. One type, called multi-infarct dementia (MID), is caused by numerous small strokes in the brain. MID typically includes multiple damaged areas, called infarcts, along with extensive lesions in the white matter, or nerve fibers, of the brain.

Because the infarcts in MID affect isolated areas of the brain, the symptoms are often limited to one side of the body or they may affect just one or a few specific functions, such as language. Neurologists call these “local” or “focal” symptoms, as opposed to the “global” symptoms seen in AD, which affect many functions and are not restricted to one side of the body.

Although not all strokes cause dementia, in some cases a single stroke can damage the brain enough to cause dementia. This condition is called single-infarct dementia. Dementia is more common when the stroke takes place on the left side (hemisphere) of the brain and/or when it involves the hippocampus, a brain structure important for memory.

Another type of vascular dementia is called Binswanger’s disease. This rare form of dementia is characterized by damage to small blood vessels in the white matter of the brain (white matter is found in the inner layers of the brain and contains many nerve fibers coated with a whitish, fatty substance called myelin). Binswanger’s disease leads to brain lesions, loss of memory, disordered cognition, and mood changes. Patients with this disease often show signs of abnormal blood pressure, stroke, blood abnormalities, disease of the large blood vessels in the neck, and/or disease of the heart valves. Other prominent features include urinary incontinence, difficulty walking, clumsiness, slowness, lack of facial expression, and speech difficulty. These symptoms, which usually begin after the age of 60, are not always present in all patients and may sometimes appear only temporarily. Treatment of Binswanger’s disease is symptomatic, and may include the use of medications to control high blood pressure, depression, heart arrhythmias, and low blood pressure. The disorder often includes episodes of partial recovery.

Another type of vascular dementia is linked to a rare hereditary disorder called CADASIL, which stands for cerebral autosomal dominant arteriopathy with subcortical infarct and leukoencephalopathy. CADASIL is linked to abnormalities of a specific gene, Notch3, which is located on chromosome 19. This condition causes multi-infarct dementia as well as stroke, migraine with aura, and mood disorders. The first symptoms usually appear in people who are in their twenties, thirties, or forties and affected individuals often die by age 65. Researchers believe most people with CADASIL go undiagnosed, and the actual prevalence of the disease is not yet known. 

Alzheimer’s disease

Alzheimer’s disease

Alzheimer’s disease is the most common cause of dementia in people aged 65 and older.

In most people, symptoms of AD appear after age 60. However, there are some early-onset forms of the disease, usually linked to a specific gene defect, which may appear as early as age 30. AD usually causes a gradual decline in cognitive abilities, usually during a span of 7 to 10 years. Nearly all brain functions, including memory, movement, language, judgment, behavior, and abstract thinking, are eventually affected.

AD is characterized by two abnormalities in the brain: amyloid plaques and neurofibrillary tangles. Amyloid plaques, which are found in the tissue between the nerve cells, are unusual clumps of a protein called beta amyloid along with degenerating bits of neurons and other cells.

Neurofibrillary tangles are bundles of twisted filaments found within neurons. These tangles are largely made up of a protein called tau. In healthy neurons, the tau protein helps the functioning of microtubules, which are part of the cell’s structural support and deliver substances throughout the nerve cell. However, in AD, tau is changed in a way that causes it to twist into pairs of helical filaments that collect into tangles. When this happens, the microtubules cannot function correctly and they disintegrate. This collapse of the neuron’s transport system may impair communication between nerve cells and cause them to die.

Researchers do not know if amyloid plaques and neurofibrillary tangles are harmful or if they are merely side effects of the disease process that damages neurons and leads to the symptoms of AD. They do know that plaques and tangles usually increase in the brain as AD progresses.

In the early stages of AD, patients may experience memory impairment, lapses of judgment, and subtle changes in personality. As the disorder progresses, memory and language problems worsen and patients begin to have difficulty performing activities of daily living, such as balancing a checkbook or remembering to take medications. They also may have visuospatial problems, such as difficulty navigating an unfamiliar route. They may become disoriented about places and times, may suffer delusions (such as the idea that someone is stealing from them or that their spouse is being unfaithful), and may become short-tempered and hostile. During the late stages of the disease, patients begin to lose the ability to control motor functions. They may have difficulty swallowing and lose bowel and bladder control. They eventually lose the ability to recognize family members and to speak. As AD progresses, it begins to affect the person’s emotions and behavior. Most people with AD eventually develop symptoms such as aggression, agitation, depression, sleeplessness, or delusions.

On average, patients with AD live for 8 to 10 years after they are diagnosed. However, some people live as long as 20 years. Patients with AD often die of aspiration pneumonia because they lose the ability to swallow late in the course of the disease.