Alzheimer’s Memory Problems Originate with Protein Clumps Floating in the Brain, Not Amyloid Plaques

Researchers at Mount Sinai School of Medicine have found that Alzheimer’s is not caused by amyloid plaques, as previously thought by many researchers......

Using a new mouse model of Alzheimer's disease, researchers at Mount Sinai School of Medicine have found that Alzheimer's pathology originates in Amyloid-Beta (Abeta) oligomers in the brain, rather than the amyloid plaques previously thought by many researchers to cause the disease.

The study, which was supported by the "Oligomer Research Consortium" of the Cure Alzheimer Fund and a MERIT Award from the Veterans Administration, appears in the journal Annals of Neurology.

"The buildup of amyloid plaques was described over 100 years ago and has received the bulk of the attention in Alzheimer's pathology," said lead author Sam Gandy, MD, PhD, Professor of Neurology and Psychiatry, and Associate Director of the Alzheimer's Disease Research Center, Mount Sinai School of Medicine. "But there has been a longstanding debate over whether plaques are toxic, protective, or inert."

Several research groups had previously proposed that rather than plaques, floating clumps of amyloid (called oligomers) are the key components that impede brain cell function in Alzheimer's patients. To study this, the Mount Sinai team developed a mouse that forms only these oligomers, and never any plaques, throughout their lives.

The researchers found that the mice that never develop plaques were just as impaired by the disease as mice with both plaques and oligomers. Moreover, when a gene that converted oligomers into plaques was added to the mice, the mice were no more impaired than they had been before.

"These findings may enable the development of neuroimaging agents and drugs that visualize or detoxify oligomers," said Dr. Gandy. "New neuroimaging agents that could monitor changes in Abeta oligomer presence would be a major advance. Innovative neuroimaging agents that will allow visualization of brain oligomer accumulation, in tandem with careful clinical observations, could lead to breakthroughs in managing, slowing, stopping or even preventing Alzheimer's.

"This is especially important in light of research reported in March showing that 70 weeks of infusion of the Abeta immunotherapeutic Bapineuzumab® cleared away 25 percent of the Abeta plaque, yet no clinical benefit was evident."

The Mount Sinai team included Michelle Ehrlich, MD, Professor of Pediatrics, Neurology, and Genetics and Genomic Sciences, and John Steele, a Mount Sinai graduate student, who performed the key analyses of the behavioral data. Dr. Charles Glabe, an oligomer expert and a member of the Cure Alzheimer Fund research consortium, is also a co-author of the paper. Dr Gandy is also a neurologist at the James J Peters Veterans Affairs Medical Center, an affiliate of Mount Sinai School of Medicine.

About The Mount Sinai Medical Center

The Mount Sinai Medical Center encompasses both The Mount Sinai Hospital and Mount Sinai School of Medicine. Established in 1968, Mount Sinai School of Medicine is one of few medical schools embedded in a hospital in the United States. It has more than 3,400 faculty in 32 departments and 15 institutes, and ranks among the top 20 medical schools both in National Institute of Health funding and by U.S. News & World Report. The school received the 2009 Spencer Foreman Award for Outstanding Community Service from the Association of American Medical Colleges.

The Mount Sinai Hospital, founded in 1852, is a 1,171-bed tertiary- and quaternary-care teaching facility and one of the nation’s oldest, largest and most-respected voluntary hospitals. In 2009, U.S. News & World Report ranked The Mount Sinai Hospital among the nation’s top 20 hospitals based on reputation, patient safety, and other patient-care factors. Nearly 60,000 people were treated at Mount Sinai as inpatients last year, and approximately 530,000 outpatient visits took place.

For more information, visit http://www.mountsinai.org/.

By Bob DeMarco
Alzheimer's Reading Room

Definition, Types and Symptoms of Multi Infarct Vascular Dementia

Multi-infarct vascular dementia is a viscious, unrelentless enemy.

As some of you may be aware, my mother suffers from advanced vascular dementia which is of the multiple infarct dementia type (thousands of mini strokes/transient ischemic attacks or TIA's as they are sometimes called).

Mum's vascular dementia was of the clot type - that is, a clot forms and clogs a blood vessel, thereby preventing cells from getting oxygen and nutrients, hence cells die. The other type of vascular dementia is of the bleeding type - a blood vessel raptures, causing a loss of blood flow to some cells, which then die.

It's important to make this distinction between these two types of vascular dementia, as in the clot type vascular dementia, one want's to thin the blood, as with half an aspirin daily, to help prevent the clots forming or doing damage. With the bleeding type vascular dementia, we want to strengthen blood vessel walls and minimise bleeding when a rapture occurs, so that more blood remains flowing in the blood vessels.

If one was to thin the blood for a bleeder type vascular dementia, it would likely cause the vascular dementia to accelerate much faster, whereas, if the same were done for a clot type vascular dementia, the vascular dementia would likely be expected to be slowed down.

The symptoms of multi-infarct vascular dementia can vary greatly from one sufferer to the next. For example, my mum was able to recall who we, her children were, well into it's advanced stages. My Aunty Myrtle, on the other hand, went more and more back into the memories of her childhood and soon lost the ability to recall who her children were and sometimes confused them with other people from her early past.

The rate of onslaught of, or deterioration from the multi-infarct vascular dementia can vary greatly from between people as well. Mum's vascular dementia slowly reaked it's destruction over many year, while Myrtle, who came down with it much later than mum, has died following the multi-infarct's much more rapid onslaught on her. Some dementia sufferers only last a few months when placed into a dementia facility - even though their dementia may not be as far advanced as others, they just seem to lose the will to live and die soon after, no matter how homely and nice and friendly the facility may be. I think it's perhaps more the separation from loved ones and carers, the change in the physical environment, that causes some dementia sufferers to just give up and die. Lets face it though, for many of those with vascular dementia or Alzheimer's Disease, there will normally come a time when the needs of the dementia sufferer exceed the abilities and or endurance of their carer to look after them.

Any way, after about 5 or 6 years, the multi-infarct vascular dementia has caused mum to become bed ridden, unable to chew, nor talk (except perhaps for yea), nor walk.

Source: www.alzheimersdementia.cdadc.com/vasculardementia.html

What is Pick's Disease and Frontal Lobe Dementia?

What is Pick's disease?

Pick's disease is a cause of dementia similar to Alzheimer's disease involving a progressive decline in a person's mental powers over a number of years. It occurs far less frequently than Alzheimer's disease, and usually starts to take effect between the ages of 40 and 65. Damage to brain cells is more localised than in Alzheimer's disease, and usually begins in the front part of the brain or frontal lobe. The initial symptoms affect personality and behaviour more and memory rather less than those of Alzheimer's. In later stages the person becomes totally dependent on others and the condition is very similar to late stage Alzheimer's. After death Pick's disease can be distinguished from Alzheimer's because there are no 'senile plaques' and characteristic changes in affected areas, known as Pick's bodies and Pick's cells, are found. The condition was first described by a German neurologist, Arnold Pick, in 1892.

What is frontal lobe dementia?

Frontal lobe dementia is the name given to any dementia caused by damage to this part of the brain. It includes Pick's disease but can also be caused by other diseases. They all have similar symptoms and prognoses.

What are the symptoms?

The frontal lobe of the brain is the part that governs our mood and behaviour. The person's mood and behaviour may become fixed and difficult to change, making them appear selfish and unfeeling. The affected person usually knows where they are, what day it is and does not have the sudden lapses of memory which are characteristic of Alzheimer's disease. Some people become withdrawn, while others lose their normal inhibitions and start talking to strangers. Others become aggressive. In many cases a person's normal sense of judgment seems to desert them. Because they lose their inhibitions and judgment some people exhibit sexual behaviour in public. The difference in symptoms between Alzheimer's disease and Pick's disease can be illustrated by thinking of different ways in which someone might walk out of a shop without paying.

In Alzheimer's disease this might happen because they become confused and forget they are holding a bag or forgot to pay.

In Pick's disease someone might know perfectly well they have the shopping but fail to see why they should be expected to pay for it. These behaviours can be very distressing for relatives and carers. They have a physical cause, and are not something that the person can usually control or contain. As the disease progresses language is affected. The person may become obsessional, repeating patterns of movement and behaviours like hand-washing, or repeating whatever is said to them. There is often an oral fixation, which can lead to people overeating and to putting objects other than food into the mouth. Some cases of Pick's disease also affect cells in the temporal lobe of the brain. When this happens memory is more likely to be affected, and the disease will more closely mimic Alzheimer's, with the addition of behavioural disorders. In the later stages the dementia is generalised. The person no longer recognises friends and family and may become totally dependent and need nursing care.

Is treatment possible?

A brain scan may help to define Pick's disease by showing the degree and location of the degeneration in the brain. There is no cure and no effective treatment yet available. The risk factors for Pick's disease are less well understood than for Alzheimer's disease. Some people with Pick's disease and frontal lobe dementia can live for a very long period of time, while others have a more rapid illness.

Is Pick's disease genetic?

Most cases of Pick's disease are not inherited or passed on to children. There is a small number of Pick's disease families where the disease is passed on in the genes. In these cases, inheriting the gene means developing the disease, often as young as 40. Some other frontal lobe dementias have a stronger genetic link.

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Should Mom Still Be Driving?

By Heather Frenette, RN, MSN, CMC

Whether or not an elderly person should be driving is a question I am frequently asked. It is a very touchy subject and most children do not want to force the issue with their parents. Getting a drivers license is a rite of passage that most teenagers look forward to. Having to give up that license can be very difficult. It affects a person’s independence. When a person has to surrender their driver’s license, they suddenly are dependent on others to get around. Going to the grocery store, going to the doctor and even going out with friends can become difficult without transportation.


There are several warning signs to look if you are concerned about a loved one’s safety behind the wheel. If you notice any of the following 17 warning signs, it is time to evaluate whether your loved one should continue driving.

1. signaling incorrectly

2. trouble making turns

3. changing lanes improperly

4. confusion at highway exits

5. difficulty parking

6. stopping inappropriately in traffic

7. confusing the brake and gas pedals

8. driving too fast or slow

9. hitting curbs

10. failing to notice stop signs or traffic lights

11. reacting slowly to traffic situations

12. failing to anticipate potential dangers

13. getting lost in familiar places

14. scrapes or dents on car, house, garage, etc.

15. traffic violations

16. near-misses

17. accidents

There are several options for driving evaluation. One option is to have an evaluation through a driving evaluation center. Although there are companies that offer these services, many of these programs are offered through larger rehabilitation centers as well. Another option is to have a physician write a letter to the Department of Motor Vehicles (DMV) expressing their concern about their patient’s driving ability. Once the DMV receives this letter, they will send out a letter to your loved one either revoking their license or requesting them to come in for a written test and/or an on the road driving test. Successful completion of the testing is necessary for the license to remain valid.

It can be hard for family members to address the topic of driving safety with their loved one. Involving the primary care physician in this process can be helpful because it takes the role away from the family. Another option is to consult with a Geriatric Care Manager. Care Managers are typically well versed in the resources to evaluate driving and can facilitate not only the testing, but also put a plan in place to address the need for transportation once the person stops driving. Again, involving an independent third party takes the pressure off the family and takes some of the emotion out of the situation.

Addressing driving concerns with your loved one can be stressful and very difficult. It is an emotional topic with significant consequences. Having a plan to both evaluate your loved one’s driving and to accommodate their transportation needs if they stop driving will help make this difficult task somewhat easier.