Here is another view of how massive cell loss changes the whole brain in advanced Alzheimer's disease. This slide shows a crosswise "slice" through the middle of the brain between the ears.
In the Alzheimer brain:
- The cortex shrivels up, damaging areas involved in thinking, planning and remembering.
- Shrinkage is especially severe in the hippocampus, an area of the cortex that plays a key role in formation of new memories.
- Ventricles (fluid-filled spaces within the brain) grow larger.
Alzheimer’s disease is a brain disorder named for German physician Alois Alzheimer, who first described it in 1906. Scientists have learned a great deal about Alzheimer’s disease in the century since Dr. Alzheimer first drew attention to it. Today we know that Alzheimer’s:
- Is a progressive and fatal brain disease. As many as 5.3 million Americans are living with Alzheimer’s disease. Alzheimer's destroys brain cells, causing problems with memory, thinking and behavior severe enough to affect work, lifelong hobbies or social life. Alzheimer’s gets worse over time, and it is fatal. Today it is the sixth-leading cause of death in the United States. For more information, see Warning Signs and Stages of Alzheimer’s Disease.
The role of plaques and tangles
Two abnormal structures called plaques and tangles are prime suspects in damaging and killing nerve cells. Plaques and tangles were among the abnormalities that Dr. Alois Alzheimer saw in the brain of Auguste D., although he called them different names.
- Plaques build up between nerve cells. They contain deposits of a protein fragment called beta-amyloid (BAY-tuh AM-uh-loyd). Tangles are twisted fibers of another protein called tau (rhymes with “wow”).
- Tangles form inside dying cells. Though most people develop some plaques and tangles as they age, those with Alzheimer’s tend to develop far more. The plaques and tangles tend to form in a predictable pattern, beginning in areas important in learning and memory and then spreading to other regions.
- Is the most common form of dementia, a general term for the loss of memory and other intellectual abilities serious enough to interfere with daily life. Alzheimer’s disease accounts for 50 to 70 percent of dementia cases. Other types of dementia include vascular dementia, mixed dementia, dementia with Lewy bodies and frontotemporal dementia. For more information about other causes of dementia, please see Related Dementias.
- Has no current cure. But treatments for symptoms, combined with the right services and support, can make life better for the millions of Americans living with Alzheimer’s. There is an accelerating worldwide effort under way to find better ways to treat the disease, delay its onset, or prevent it from developing. Learn more about recent progress in Alzheimer research funded by the Alzheimer’s Association in the Research section.
Last Updated: Sunday, 29 April 2007, 21:10 GMT 22:10 UK
The study says progress is possible even after major brain damage
Scientists found mice with a similar condition to Alzheimer's were able to regain memories of tasks they had previously been taught.
A team at the Massachusetts Institute of Technology found two methods - brain stimulation and drugs - both worked.
Their findings were published in British journal Nature.
The researchers used genetically engineered mice in which a protein linked to degenerative brain disease could be triggered.
Scientists had previously given the mice tests where they learnt to avoid an electric shock and how to find their way through a maze to reach food.
After six weeks with the brain disease, the mice were no longer able to remember how to perform these tasks.
Some of the mice were then placed in a more stimulating environment with toys, treadmills and other mice.
The playground mice were able to remember the shock test far better than the mice in other cages. They were also better at learning new things.
Scientists then tested a class of drugs called histone deacetylase, or HDAC, inhibitors on the mice.
These also improved memory and learning, similar to improvements made by environmental stimulation.
Neuroscientist Li-Huei Tsai of the Howard Hughes Medical Institute and the Massachusetts Institute of Technology said the results could offer hope to people with diseases like Alzheimer's.
"We show the first evidence that even if the brain suffered some very severe neurodegeneration and the individual exhibits very severe learning impairment and memory loss, there is still the possibility to improve learning ability and recover to a certain extent lost long-term memories."
She said the study suggested that in people with degenerative brain diseases, memories were not erased from the brain, but rather could not be accessed because of the disease.
She added that while most treatments for Alzheimer's targeted the disease's early stages, this research showed that even after major brain damage it was still possible to improve learning and memory.
Dr Susanne Sorensen, head of research, Alzheimer's Society, said: "These results cannot automatically be translated to people and a lot more has to be done to narrow the focus on the processes that are involved.
"However, by demonstrating that lost memories can be accessed again these results offer hope of a better understanding of what happens to memories as dementia develops."It highlights the role of both an 'enriching environment' and through its focus on biochemical processes could provide important building blocks for new treatments to alleviate the symptoms of dementia."
last updated at 23:53 GMT, Wednesday, 6 May 2009 00:53 UK
Trial drugs 'reverse' Alzheimer's
US scientists say they have successfully reversed the effects of Alzheimer's with experimental drugs.
The drugs target and boost the function of a newly pinpointed gene involved in the brain's memory formation.
In mice, the treatment helped restore long-term memory and improve learning for new tasks, Nature reports.
The same drugs - HDAC inhibitors - are currently being tested to treat Huntington's disease and are on the market to treat some cancers.
They reshape the DNA scaffolding that supports and controls the expression of genes in the brain.
The Alzheimer's gene the drugs act upon, histone deacetylase 2 (HDAC2), regulates the expression of a plethora of genes implicated in plasticity - the brain's ability to change in response to experience - and memory formation.
This findings build on the team's 2007 breakthrough in which mice with symptoms of Alzheimer's disease regained long-term memories and the ability to learn.
Lead researcher Professor Li-Huei Tsai explained: "It brings about long-lasting changes in how other genes are expressed, which is probably necessary to increase numbers of synapses and restructure neural circuits, thereby enhancing memory.
"To our knowledge, HDAC inhibitors have not been used to treat Alzheimer's disease or dementia.
"But now that we know that inhibiting HDAC2 has the potential to boost synaptic plasticity, synapse formation and memory formation.
"In the next step, we will develop new HDAC2-selective inhibitors and test their function for human diseases associated with memory impairment to treat neurodegenerative diseases."
HDAC inhibitor treatment for humans with Alzheimer's disease is still a decade or more away, she said.
The chief executive of the Alzheimer's Research Trust, Rebecca Wood, said: "This is promising research which improves our understanding of memory loss in Alzheimer's.
"We need to do more research to investigate whether developing treatments that control this gene could benefit people with Alzheimer's.
"We desperately need to fund more research to head off a forecast doubling the UK population living with dementia."
Julie Williams, an expert in the genetics of Alzheimer's for the trust, said scientists were on the brink of finding a number of candidate genes that increase the risk of developing Alzheimer's.
"If we can find the triggers and causes then we can hopefully prevent them. That is the great ambition."
Remembering My Friend Muriel