Posts

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. 

Related Articles:

Please leave your thoughts and comments

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

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.”


Story Source:

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.

Dementia 101: Types of Dementia

Dementia, Alzheimer’s, senility, forgetfulness. All of these words point to an experience. But do they point to the same one? Are they different? Are they the same?

I often hear these words thrown around interchangeably. Here I hope to give some etymological clarity. Aging in America is confusing. By using clear language, I hope we can communicate more effectively about our experiences. Through sharing experiences we also share wisdom to age more playfully.

I work in the field of psychology, which uses the DSM as its diagnostic manual. It is based on this that I will share the different types of dementia, or as it is now clinically called, neurocognitive disorder.

This brings us to our first language issue — dementia or NCD are interchangeable and are overarching terms for all that will follow. Below are all types of dementia or subtypes of NCD.

After someone is determined to be experiencing dementia, a subtype allows the experience to be further defined according to the known or presumed cause as well as the main characteristics, timeline, and symptom set of the dementia.

Knowing a subtype can help give behaviors meaning and offer understanding, as well as offering a way to share best practices for living with dementia. There is a wealth of research on each of these. Below is a very basic overview meant to be used as a starting point of understanding.

2015-06-12-1434132834-8593985-typesofdementia.jpg

1. Alzheimer’s disease — Alzheimer’s is named for the doctor who found the pathologies believed to be the cause. Although the exact cause for the behaviors labeled as Alzheimer’s is still unknown, it is thought to be inherited genetically. Alzheimer’s varies from other dementias in that it’s progression is steady and gradual. For a diagnosis of probable Alzheimer’s (probable because the tangles from which its name is derived can only be verified during a postmortem brain autopsy) there must be a decline in memory, learning and one other domain.

2. Frontal Temporal Dementia (FTD) or Frontotemporal lobar degeneration — This dementia is named for the part of the brain it affects most — the frontal lobe. FTD seems to appear suddenly and then progresses gradually. There is a behavioral and language variant. The behavioral variant is marked by disinhibition and changes in social behavior. The language variant results in a dramatic change in language ranging from speech production to word comprehension.

3. Lewy Body Disease — This type is also named for its assumptive cause — lewy bodies in the brain. Those with Lewy Body disease experience fluctuating cognition levels. This disease is also marked by detailed visual hallucinations. These hallucinations are not psychosis. Unfortunately, antipsychotics are often given to treat these hallucinations. These drugs are contraindicated or not recommended for people with a Lewy Body diagnosis and can make symptoms worsen. Lewy Body also has features of parkinsonism. There are more physical changes associated with Lewy Body than other dementias.

The remaining types are named for their cause; their exact symptoms vary based on the area of the brain which was damaged and how extensive the damage is. 

4. NCD due to vascular disease — The onset usually coincides with a cerebrovascular event — a disruption of blood supply to the brain, such as a stoke.

5. NCD due to traumatic brain injury — There must be evidence of an injury to the brain such as an impact to the head, either at a single moment or repeated over time such as multiple concussions from playing a contact sport.

6. Substance or medication induced — Damage has been done to the brain through the use of substances or medication. The symptoms remain after usual duration of intoxication or withdrawal.

7. Due to HIV infection — There is evidence of HIV infection and the dementia is not better attributed to another type.

8. Due to Prion disease — There is evidence of prion disease as well as rapid progression of NCD symptoms.

9. Due to Parkinson’s Disease — Parkinson’s is present before the NCD.

10. Due to Huntington’s Disease — Huntington’s is diagnosed before NCD, or there is family history or genetic testing to support the diagnosis.

In addition to these 10 types there are also the diagnoses of “NCD due to another medical condition” as well as “NCD due to multiple etiologies,” meaning that more than one of these types are present at the same time.

Every person is unique and so is their experience of dementia.

Understanding these broad categories can help us to share experiences and find helpful resources. Only a medical doctor or licensed mental health professional can offer a diagnosis. These same people can be very helpful in connecting you to local resources such as support groups, therapeutics, educational programs and medical resources.

What is dementia? The signs, symptoms and causes of dementia

Dementia is a term used to describe various symptoms of cognitive decline such as forgetfulness, but is not a clinical diagnosis itself until an underlying disease or disorder has been identified.

Dementia is a collective term used to describe the problems that people with various underlying brain disorders or damage can have with their memory, language and thinking. Alzheimer’s disease is the best known and most common disorder under the umbrella of dementia.

What is dementia?

Dementia is not a single disease in itself, but a general term to describe symptoms such as impairments to memory, communication and thinking.1

While the likelihood of having dementia increases with age, it is not a normal part of aging. Before we had today’s understanding of specific disorders, “going senile” used to be a common phrase for dementia (“senility”), which misunderstood it as a standard part of getting old. 1,2

Light cognitive impairments, by contrast, such as poorer short-term memory, can happen as a normal part of aging (we slowly start to lose brain cells as we age beyond our 20s3). This is known as age-related cognitive decline, not dementia, because it does not cause the person or the people around them any problems.1 Dementia describes two or more types of symptom that are severe enough to affect daily activities.

Symptoms that are classed as “mild cognitive impairment” – which, unlike cognitive decline, are not a normal part of aging – do not qualify as dementia either, since these symptoms are not severe enough.1 For some people though, this milder disease leads to dementia later on.4

A number of brain disorders with more severe symptoms are classified as dementias, with Alzheimer’s disease being the best known and most common.

An analysis of the most recent census estimates that 4.7 million people aged 65 years or older in the US were living with Alzheimer’s disease in 2010.5 The Alzheimer’s Association has used this analysis to number-crunch the extent of the disorder in its 2013 report. It estimates that:

  • Just over a tenth of people aged 65 years or more have Alzheimer’s disease
  • This proportion rises to about a third of people aged 85 and older.

The non-profit organization says Alzheimer’s accounts for between 60% and 80% of all cases of dementia, with vascular dementia caused by stroke being the second most common type.

What causes dementia?

All dementias are caused by brain cell death,1 and neurodegenerative disease – progressive brain cell death that happens over a course of time – is behind most dementias.4,6

brain neuron
Nerve cells (neurons) in the brain – loss or damage can cause dementia. Alzheimer’s disease is the leading cause.

But as well as progressive brain cell death like that seen in Alzheimer’s disease, dementia can be caused by a head injury, a stroke or a brain tumor, among other causes.6

Some of the causes are simpler to understand in terms of how they affect the brain and lead to dementia:1

  • Vascular dementia – this results from brain cell death caused by conditions such as cerebrovascular disease, for example stroke. This prevents normal blood flow, depriving brain cells of oxygen.
  • Injury – post-traumatic dementia is directly related to brain cell death caused by injury.

Some types of traumatic brain injury – particularly if repetitive, such as received by sports players – have been linked to certain dementias appearing later in life. Evidence is weak, however, that a single brain injury will raise the likelihood of having a degenerative dementia such as Alzheimer’s disease.7

Dementia can also be caused by:1,2,8

  • Prion diseases – from certain types of protein, as in CJD (Creutzfeldt-Jakob disease) and GSS (Gerstmann-Straussler-Scheinker syndrome).
  • HIV infection – when the problem is simply termed HIV-associated dementia. How the virus damages brain cells is not certain.
  • Reversible factors – some dementias can be treated by reversing the effects of underlying causes, including medication interactions, depressionvitamin deficiencies (for example, thiamine/B1, leading to Wernicke-Korsakoff syndrome, which is most often caused by alcohol misuse), and thyroid abnormalities.

Alzheimer’s dementia is caused by progressive brain cell death. Estimates range between 60% and 80% for the proportion of all cases of dementia being accounted for by Alzheimer’s disease.2 In the US, about 5.3 million people are thought to have the disorder among the estimated 6.8 million individuals who have some form of dementia.4

Alzheimer’s is thought to be caused by “plaques” between the dying cells in the brain and “tangles” within the cells (both are protein abnormalities: a build-up of “beta-amyloid” in plaques and the disintegration of “tau” protein in tangles).

These inclusions in the brain are always present with the disorder but whether they are themselves the cause, or if there is some other underlying process, is not known – and there is some overlap with other disorders that show similar changes in brain cells.1,9

The brain tissue in a person with Alzheimer’s has progressively fewer nerve cells and connections, and the total brain size shrinks.1,9

See the Medical News Today Alzheimer’s disease page for more detailed information about this specific type of dementia.

Dementia with Lewy bodies is also caused by neurodegeneration linked to abnormal structures in the brain. Here, the brain changes involve a protein called alpha-synuclein.10

Mixed dementia refers to a diagnosis of two or three types occurring together. A person may show both Alzheimer’s disease and vascular dementia at the same time. Or the combination could be Lewy bodies and Alzheimer’s. There can also be a combination of all three types.10

Parkinson’s disease is also marked by the presence of Lewy bodies. While the part of the brain affected means there are classic movement symptoms, people with Parkinson’s can also go on to develop dementia symptoms as the degenerative changes in the brain gradually spread.10

Huntington’s disease is similar to Parkinson’s in the respect of being classically marked by uncontrolled movements yet having dementia as a component. It results in mood changes, too. Huntington’s is an inherited condition caused by a single faulty gene. This can produce the disease at any age – as young at 2 years of age and as old as 80, but typically between the ages of 30 and 50 years.10

Other disorders leading to symptoms of dementia include:10

  • Frontotemporal dementia (also known as Pick’s disease)
  • Normal pressure hydrocephalus (when excess cerebrospinal fluid accumulates in the brain)
  • Posterior cortical atrophy (caused by the same tissue abnormalities seen in Alzheimer’s disease, but in a different part of the brain), and
  • Down syndrome (people born with this are more likely to develop young-onset Alzheimer’s).

Recent developments on causes of dementia from MNT news

Link found between dementia and vitamin D deficiency – In what is regarded as the first large, population-based study of its kind, a team of researchers has found a link between vitamin D consumption and the risk of developing dementia. Older people who do not get enough vitamin D could double their risk of developing the condition.

Traumatic brain injury in older adults linked to increased dementia risk – A study published in JAMA Neurologysuggests that for adults aged 55 years and older, traumatic brain injury may be linked to an increased risk of dementia.

Does poor sleep increase risk of dementia? – While sleep protects both physical and mental health, some people experience better sleep than others. Now, new research has associated poor sleep with an increased risk of dementia as a result of changes that occur within the brain.

Signs and symptoms

mature lady looking confused
Memory loss in dementia can be serious enough for the person to forget where they are, even on their home street.

The symptoms of dementia experienced by patients, or noticed by people close to them, are exactly the same signs that healthcare professionals look for. Therefore, detailed information on these is given in the next section about tests and diagnosis.

A person with dementia may show any of the following problems, mostly due to memory loss – some of which they may notice (or become frustrated with) themselves, while others may only be picked up by carers or healthcare workers as a cause for concern. The signs used to compile this list are published by the American Academy of Family Physicians (AAFP) in the journal American Family Physician:6

  • Recent memory loss – a sign of this might be asking the same question repeatedly, forgetting about already asking it.
  • Difficulty completing familiar tasks – for example, making a drink or cooking a meal, but forgetting and leaving it.
  • Problems communicating – difficulty with language by forgetting simple words or using the wrong ones.
  • Disorientation – with time and place, getting lost on a previously familiar street close to home, for example, and forgetting how they got there or would get home again.
  • Poor judgment – the AAFP says: “Even a well person might get distracted and forget to watch a child for a little while. People with dementia, however, might forget all about the child and just leave the house for the day.”
  • Problems with abstract thinking – for example, dealing with money.
  • Misplacing things – including putting them in the wrong places and forgetting about doing this.
  • Mood changes – unlike those we all have, swinging quickly through a set of moods.
  • Personality changes – becoming irritable, suspicious or fearful, for example.
  • Loss of initiative – showing less interest in starting something or going somewhere.

The Alzheimer’s Association has put together Know the 10 signs – a PDF document listing real-life examples of how this type of dementia can affect people.

What causes dementia

All dementias are caused by brain cell death,1 and neurodegenerative disease – progressive brain cell death that happens over a course of time – is behind most dementias.4,6

brain neuron
Nerve cells (neurons) in the brain – loss or damage can cause dementia. Alzheimer’s disease is the leading cause.

But as well as progressive brain cell death like that seen in Alzheimer’s disease, dementia can be caused by a head injury, a stroke or a brain tumor, among other causes.6

Some of the causes are simpler to understand in terms of how they affect the brain and lead to dementia:1

  • Vascular dementia – this results from brain cell death caused by conditions such as cerebrovascular disease, for example stroke. This prevents normal blood flow, depriving brain cells of oxygen.
  • Injury – post-traumatic dementia is directly related to brain cell death caused by injury.

Some types of traumatic brain injury – particularly if repetitive, such as received by sports players – have been linked to certain dementias appearing later in life. Evidence is weak, however, that a single brain injury will raise the likelihood of having a degenerative dementia such as Alzheimer’s disease.7

Dementia can also be caused by:1,2,8

  • Prion diseases – from certain types of protein, as in CJD (Creutzfeldt-Jakob disease) and GSS (Gerstmann-Straussler-Scheinker syndrome).
  • HIV infection – when the problem is simply termed HIV-associated dementia. How the virus damages brain cells is not certain.
  • Reversible factors – some dementias can be treated by reversing the effects of underlying causes, including medication interactions, depressionvitamin deficiencies (for example, thiamine/B1, leading to Wernicke-Korsakoff syndrome, which is most often caused by alcohol misuse), and thyroid abnormalities.

Alzheimer’s dementia is caused by progressive brain cell death. Estimates range between 60% and 80% for the proportion of all cases of dementia being accounted for by Alzheimer’s disease.2 In the US, about 5.3 million people are thought to have the disorder among the estimated 6.8 million individuals who have some form of dementia.4

Alzheimer’s is thought to be caused by “plaques” between the dying cells in the brain and “tangles” within the cells (both are protein abnormalities: a build-up of “beta-amyloid” in plaques and the disintegration of “tau” protein in tangles).

These inclusions in the brain are always present with the disorder but whether they are themselves the cause, or if there is some other underlying process, is not known – and there is some overlap with other disorders that show similar changes in brain cells.1,9

The brain tissue in a person with Alzheimer’s has progressively fewer nerve cells and connections, and the total brain size shrinks.1,9

See the Medical News Today Alzheimer’s disease page for more detailed information about this specific type of dementia.

Dementia with Lewy bodies is also caused by neurodegeneration linked to abnormal structures in the brain. Here, the brain changes involve a protein called alpha-synuclein.10

Mixed dementia refers to a diagnosis of two or three types occurring together. A person may show both Alzheimer’s disease and vascular dementia at the same time. Or the combination could be Lewy bodies and Alzheimer’s. There can also be a combination of all three types.10

Parkinson’s disease is also marked by the presence of Lewy bodies. While the part of the brain affected means there are classic movement symptoms, people with Parkinson’s can also go on to develop dementia symptoms as the degenerative changes in the brain gradually spread.10

Huntington’s disease is similar to Parkinson’s in the respect of being classically marked by uncontrolled movements yet having dementia as a component. It results in mood changes, too. Huntington’s is an inherited condition caused by a single faulty gene. This can produce the disease at any age – as young at 2 years of age and as old as 80, but typically between the ages of 30 and 50 years.10

Other disorders leading to symptoms of dementia include:10

  • Frontotemporal dementia (also known as Pick’s disease)
  • Normal pressure hydrocephalus (when excess cerebrospinal fluid accumulates in the brain)
  • Posterior cortical atrophy (caused by the same tissue abnormalities seen in Alzheimer’s disease, but in a different part of the brain), and
  • Down syndrome (people born with this are more likely to develop young-onset Alzheimer’s).

Recent developments on causes of dementia from MNT news

Link found between dementia and vitamin D deficiency – In what is regarded as the first large, population-based study of its kind, a team of researchers has found a link between vitamin D consumption and the risk of developing dementia. Older people who do not get enough vitamin D could double their risk of developing the condition.

Traumatic brain injury in older adults linked to increased dementia risk – A study published in JAMA Neurologysuggests that for adults aged 55 years and older, traumatic brain injury may be linked to an increased risk of dementia.

Does poor sleep increase risk of dementia? – While sleep protects both physical and mental health, some people experience better sleep than others. Now, new research has associated poor sleep with an increased risk of dementia as a result of changes that occur within the brain.

Signs and symptoms

mature lady looking confused
Memory loss in dementia can be serious enough for the person to forget where they are, even on their home street.

The symptoms of dementia experienced by patients, or noticed by people close to them, are exactly the same signs that healthcare professionals look for. Therefore, detailed information on these is given in the next section about tests and diagnosis.

A person with dementia may show any of the following problems, mostly due to memory loss – some of which they may notice (or become frustrated with) themselves, while others may only be picked up by carers or healthcare workers as a cause for concern. The signs used to compile this list are published by the American Academy of Family Physicians (AAFP) in the journal American Family Physician:6

  • Recent memory loss – a sign of this might be asking the same question repeatedly, forgetting about already asking it.
  • Difficulty completing familiar tasks – for example, making a drink or cooking a meal, but forgetting and leaving it.
  • Problems communicating – difficulty with language by forgetting simple words or using the wrong ones.
  • Disorientation – with time and place, getting lost on a previously familiar street close to home, for example, and forgetting how they got there or would get home again.
  • Poor judgment – the AAFP says: “Even a well person might get distracted and forget to watch a child for a little while. People with dementia, however, might forget all about the child and just leave the house for the day.”
  • Problems with abstract thinking – for example, dealing with money.
  • Misplacing things – including putting them in the wrong places and forgetting about doing this.
  • Mood changes – unlike those we all have, swinging quickly through a set of moods.
  • Personality changes – becoming irritable, suspicious or fearful, for example.
  • Loss of initiative – showing less interest in starting something or going somewhere.

The Alzheimer’s Association has put together Know the 10 signs – a PDF document listing real-life examples of how this type of dementia can affect people.