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Alzheimer's disease is a form of dementia that severely decays a person's memory and ability to complete common activities progressively as they age.  Currently, the disease isn't curable though treatment is available.

My interest towards researching the topic emerged after witnessing the progressing affects of the disease upon my grandmother.

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In 1906, the German physician noticed changes in the brain tissue of a patient who died from a mental illness, including symptoms of memory loss, difficulties speaking, and unpredictable behavior.

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In 1910, the German psychiatrist first names Alzheimer's disease after fellow colleague, Dr. Alois Alzheimer.

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Senile Plagues
An extracellular collection of proteins known as amyloid beta, senile plaques accumulate and cause damage to areas of the brain such as the hippocampus.

Neurofibrillary Tangles
Insoluble twisted fibers found inside the brain's cells and are formed from a clump of tau proteins; functions similarly as amyloid beta in regards to cellular damage.

Acetylcholine Deficit
View suggests Alzheimer's is the result of insufficient synthesis of the neurotransmitter acetylcholine.

Oxidative Stress
Process in which high reactive molecules known as free radicals damage cellular structures; propagates Alzheimer's by facilitating damage caused by amyloid beta and enhances its formation.

Inflammation
Results in damaged neurons and is facilitated by tumor necrosis factor-alpha (TNF-a).  TNF-a is a pro-inflammatory cytokine, cell signalling molecules that stimulate the movement of cells towards sites (notably inflammation), that is found in high levels in serum and cerebral spinal fluid.

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Mitochondrial Dysfunction
Dysfunctional mitochondria are crucial mediators of amyloid beta toxicity and can increase the burden of oxidative stress; drives the formation of amyloid beta, ultimately leading to the destruction of neurons.

Excitotoxicity
The result of too much glutamatergic neurotransmission can destroy neurons and is a phenomenon known as excitotoxicity; contributes to neural degeneration in Alzheimer's and is the result of the over activation of N-methyl-D-aspartate receptors.

Loss of Sex Hormones
Declining estrogen and testosterone levels are correlated with increased amyloid beta and tau abnormalities; furthermore, a decline in sex hormones weakens the protection of an individual against the disease.

Infections
Research indicates common pathogens, such as Spirochetes, are constantly detected in the brain of Alzheimer's patients. As a result of lingering in the brain, bacteria can drive inflammation and form amyloid beta and neurofibrillary tangles. In fact, the research indicates amyloid beta's formation to be an adaptive response to infectious organisms.

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Further Information About Abnormal Psychology...

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Further Information About Abnormal Psychology...

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How Psychologists Define and Study Abnormal Psychology

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Abnormal psychology focuses on abnormal behavior, psychopathology, and psychological disorders. However, psychologists struggle to define the term abnormal.

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(original) Man In Nursing Home Reacts To Hearing Music From His Era

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Targeting Plaques

-Recruit the immune system through solanezumab and Aducanumab (current drugs under research.

-Prevent destruction of nerve cells in the brain by administering the drug saracatinib, which has been found to turn off the protein Flynn, allowing synapses to function and reverse memory loss.

-Block the production of beta-amyloid through beta- and gamma-secretase inhibitors.

Prevent Tau from Tangling
-Aggregation inhibitors and tau vaccines are under study.

Reducing Inflammation
-Administer the diabetes drug pioglitazone since it may lessen beta-amyloid and inflammation in the brain.

Insulin Resistance
-Researchers are currently testing insulin to determine if the hormone slows the progression of Alzheimer's.

Heart-Head Connection
-Researchers are currently investigating drugs used to treat vascular disease, such as blood pressure medications, in order find current developed and approved drugs that may reduce the risk of developing the disease.

Hormones
-Estrogen-based hormone therapy for at least a year during menopause appeared to protect the processing and memory capabilities of women with higher risks of developing the disease.

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Alzheimer's treatments: What's on the horizon?

Despite many promising leads, new treatments for Alzheimer's are slow to emerge.
By Mayo Clinic Staff
Current Alzheimer's treatments temporarily improve symptoms of memory loss and problems with thinking and reasoning.

These Alzheimer's treatments boost the performance of chemicals in the brain that carry information from one brain cell to another. They include cholinesterase inhibitors and the medicine memantine (Namenda). However, these treatments don't stop the underlying decline and death of brain cells. As more cells die, Alzheimer's disease continues to progress.

Experts are cautious but hopeful about developing treatments that can stop or delay the progression of Alzheimer's. Experts continue to better understand how the disease changes the brain. This has led to the research of potential Alzheimer's treatments that may affect the disease process.

Future Alzheimer's treatments may include a combination of medicines. This is similar to treatments for many cancers or HIV/ AIDS that include more than one medicine.

These are some of the strategies currently being studied.

Taking aim at plaques

Some of the new Alzheimer's treatments target clumps of the protein beta-amyloid, known as plaques, in the brain. Plaques are a characteristic sign of Alzheimer's disease.

Strategies aimed at beta-amyloid include:

Recruiting the immune system. Medicines known as monoclonal antibodies may prevent beta-amyloid from clumping into plaques. They also may remove beta-amyloid plaques that have formed. They do this by helping the body clear them from the brain. These medicines mimic the antibodies your body naturally produces as part of your immune system's response to foreign invaders or vaccines.

In 2023, the U.S. Food and Drug Administration (FDA) approved lecanemab (Leqembi) for people with mild Alzheimer's disease and mild cognitive impairment due to Alzheimer's disease.

A phase 3 clinical trial found that the medicine slowed cognitive decline in people with early Alzheimer's disease. The medicine prevents amyloid plaques in the brain from clumping. The phase 3 trial was the largest so far to study whether clearing clumps of amyloid plaques from the brain can slow the disease.

Lecanemab is given as an IV infusion every two weeks. Your care team likely will watch for side effects and ask you or your caregiver how your body reacts to the drug. Side effects of lecanemab include infusion-related reactions such as fever, flu-like symptoms, nausea, vomiting, dizziness, changes in heart rate and shortness of breath.

Also, people taking lecanemab may have swelling in the brain or may get small bleeds in the brain. Rarely, brain swelling can be serious enough to cause seizures and other symptoms. Also in rare instances, bleeding in the brain can cause death. The FDA recommends getting a brain MRI before starting treatment. It also recommends being monitored with brain MRI s during treatment for symptoms of brain swelling or bleeding.

People who carry a certain form of a gene known as APOE e4 appear to have a higher risk of these serious complications. The FDA recommends being tested for this gene before starting treatment with lecanemab.

If you take a blood thinner or have other risk factors for brain bleeding, talk to your health care professional before taking lecanemab. Blood-thinning medicines may increase the risk of bleeds in the brain.

More research is being done on the potential risks of taking lecanemab. Other research is looking at how effective lecanemab may be for people at risk of Alzheimer's disease, including people who have a first-degree relative, such as a parent or sibling, with the disease.

Another medicine being studied is donanemab. It targets and reduces amyloid plaques and tau proteins. It was found to slow declines in thinking and functioning in people with early Alzheimer's disease.

Aducanumab (Aduhelm) has been approved for the treatment of Alzheimer's disease in some people, but it's not widely used. Results were mixed in studies about how effective aducanumab is at slowing cognitive decline. Insurance coverage of the medicine is limited.

The monoclonal antibody solanezumab did not show benefits for individuals with preclinical, mild or moderate Alzheimer's disease. Solanezumab did not lower beta-amyloid in the brain, which may be why it wasn't effective.

Preventing destruction. A medicine initially developed as a possible cancer treatment - saracatinib - is now being tested in Alzheimer's disease.

In mice, saracatinib turned off a protein that allowed synapses to start working again. Synapses are the tiny spaces between brain cells through which the cells communicate. The animals in the study experienced a reversal of some memory loss. Human trials for saracatinib as a possible Alzheimer's treatment are now underway.

Production blockers. These therapies may reduce the amount of beta-amyloid formed in the brain. Research has shown that beta-amyloid is produced from a "parent protein" in two steps performed by different enzymes.

Several experimental medicines aim to block the activity of these enzymes. They're known as beta- and gamma-secretase inhibitors. Recent studies showed that the beta-secretase inhibitors did not slow cognitive decline. They also were associated with significant side effects in those with mild or moderate Alzheimer's. This has decreased enthusiasm for the medicines.

Keeping tau from tangling

A vital brain cell transport system collapses when a protein called tau twists into tiny fibers. These fibers are called tangles. They are another common change in the brains of people with Alzheimer's. Researchers are looking at a way to prevent tau from forming tangles.

Tau aggregation inhibitors and tau vaccines are currently being studied in clinical trials.

Reducing inflammation

Alzheimer's causes chronic, low-level brain cell inflammation. Researchers are studying ways to treat the processes that lead to inflammation in Alzheimer's disease. The medicine sargramostim (Leukine) is currently in research. The medicine may stimulate the immune system to protect the brain from harmful proteins.

Researching insulin resistance

Studies are looking into how insulin may affect the brain and brain cell function. Researchers are studying how insulin changes in the brain may be related to Alzheimer's. However, a trial testing of an insulin nasal spray determined that the medicine wasn't effective in slowing the progression of Alzheimer's.

Studying the heart-head connection

Growing evidence suggests that brain health is closely linked to heart and blood vessel health. The risk of developing dementia appears to increase as a result of many conditions that damage the heart or arteries. These include high blood pressure, heart disease, stroke, diabetes and high cholesterol.

A number of studies are exploring how best to build on this connection. Strategies being researched include:

Current medicines for heart disease risk factors. Researchers are looking into whether blood pressure medicines may benefit people with Alzheimer's. They're also studying whether the medicines may reduce the risk of dementia.

Medicines aimed at new targets. Other studies are looking more closely at how the connection between heart disease and Alzheimer's works at the molecular level. The goal is to find new potential medicines for Alzheimer's.

Lifestyle choices. Research suggests that lifestyle choices with known heart benefits may help prevent Alzheimer's disease or delay its onset. Those lifestyle choices include exercising on most days and eating a heart-healthy diet.

Hormones

Studies during the 1990s suggested that taking hormone replacement therapy during perimenopause and menopause lowered the risk of Alzheimer's disease. But further research has been mixed. Some studies found no cognitive benefit of taking hormone replacement therapy. More research and a better understanding of the relationship between estrogen and cognitive function are needed.

Speeding treatment development

Developing new medicines is a slow process. The pace can be frustrating for people with Alzheimer's and their families who are waiting for new treatment options.

To help speed discovery, the Critical Path for Alzheimer's Disease (CPAD) consortium created a first-of-its-kind partnership to share data from Alzheimer's clinical trials. CPAD's partners include pharmaceutical companies, nonprofit foundations and government advisers. CPAD was formerly called the Coalition Against Major Diseases.

CPAD also has collaborated with the Clinical Data Interchange Standards Consortium to create data standards. Researchers think that data standards and sharing data from thousands of study participants will speed development of more-effective therapies.

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Show references

1. Treatments and research. Alzheimer's Association. https://www.alz.org/alzheimers-dementia/research_progress/treatment-horizon. Accessed March 23, 2023.

2. Cummings J, et al. Alzheimer's disease drug development pipeline: 2022. Alzheimer's and Dementia. 2022; doi:10.1002/trc2.12295.

3. Burns S, et al. Therapeutics of Alzheimer's disease: Recent developments. Antioxidants. 2022; doi:10.3390/antiox11122402.

4. Plascencia-Villa G, et al. Lessons from antiamyloid-beta immunotherapies in Alzheimer's disease. Handbook of Clinical Neurology. 2023; doi:10.1016/B978-0-323-85555-6.00019-9.

5. Brockmann R, et al. Impacts of FDA approval and Medicare restriction on antiamyloid therapies for Alzheimer's disease: Patient outcomes, healthcare costs and drug development. The Lancet Regional Health. 2023; doi:10.1016/j.lana.2023.100467.

6. Wojtunik-Kulesza K, et al. Aducanumab - Hope or disappointment for Alzheimer's disease. International Journal of Molecular Sciences. 2023; doi:10.3390/ijms24054367.

7. Can Alzheimer's disease be prevented? Alzheimer's Association. http://www.alz.org/research/science/alzheimers_prevention_and_risk.asp. Accessed March 23, 2023.

8. Piscopo P, et al. A systematic review on drugs for synaptic plasticity in the treatment of dementia. Ageing Research Reviews. 2022; doi:10.1016/j.arr.2022.101726.

9. Facile R, et al. Use of Clinical Data Interchange Standards Consortium (CDISC) standards for real-world data: Expert perspectives from a qualitative Delphi survey. JMIR Medical Informatics. 2022; doi:10.2196/30363.

10. Imbimbo BP, et al. Role of monomeric amyloid-beta in cognitive performance in Alzheimer's disease: Insights from clinical trials with secretase inhibitors and monoclonal antibodies. Pharmacological Research. 2023; doi:10.1016/j.phrs.2022.106631.

11. Conti Filho CE, et al. Advances in Alzheimer's disease's pharmacological treatment. Frontiers in Pharmacology. 2023; doi:10.3389/fphar.2023.1101452.

12. Potter H, et al. Safety and efficacy of sargramostim (GM-CSF) in the treatment of Alzheimer's disease. Alzheimer's and Dementia. 2021; doi:10.1002/trc2.12158.

13. Zhong H, et al. Effect of peroxisome proliferator-activated receptor-gamma agonists on cognitive function: A systematic review and meta-analysis. Biomedicines. 2023; doi:10.3390/biomedicines11020246.

14. Grodstein F. Estrogen and cognitive function. https://www.uptodate.com/contents/search. Accessed March 23, 2023.

15. Mills ZB, et al. Is hormone replacement therapy a risk factor or a therapeutic option for Alzheimer's disease? International Journal of Molecular Sciences. 2023; doi:10.3390/ijms24043205.

16. Custodia A, et al. Biomarkers assessing endothelial dysfunction in Alzheimer's disease. Cells. 2023; doi:10.3390/cells12060962.

17. Overview. Critical Path for Alzheimer's Disease. https://c-path.org/programs/cpad/. Accessed March 29, 2023.

18. Shi M, et al. Impact of anti-amyloid-β monoclonal antibodies on the pathology and clinical profile of Alzheimer's disease: A focus on aducanumab and lecanemab. Frontiers in Aging and Neuroscience. 2022; doi:10.3389/fnagi.2022.870517.

19. Leqembi (approval letter). Biologic License Application 761269. U.S. Food and Drug Administration. https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=761269. Accessed July 7, 2023.

20. Van Dyck CH, et al. Lecanemab in early Alzheimer's disease. New England Journal of Medicine. 2023; doi:10.1056/NEJMoa2212948.

21. Leqembi (prescribing information). Eisai; 2023. https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&varApplNo=761269. Accessed July 10, 2023.

See more In-depth

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What new Alzheimer's treatments are on the horizon?

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Alzheimer's treatments now being studied include an Alzheimer's vaccine and several new medicines.

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Treatments for Alzheimer's is based off the following stages:

Mild Stage
-Rivastigmine
-Galantamine
-Donepezil

Moderate Stage
-Memantine

Severe Stage
-Donepezil

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Controversy: Is Alzheimer's Disease a Transmissible Infection?  

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Controversy: Is Alzheimer's Disease a Transmissible Infection?  

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Findings of a study of eight adults, aged between 36 and 51, found seven of them harbored misfolded proteins, including amyloid-beta, after receiving contaminated hormone injections.  Most importantly to note, the impact of the study raises questions towards the controversial claim of the transmission of Alzheimer's disease, as infected surgical equipment and human tissue are able to carry amyloid-beta, despite the sterilization methods of steaming and formaldehyde

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The "seeds" of Alzheimer's disease may be transmitted from one person to another during certain medical procedures - possibly including blood transfusions and dental treatment - following a study into people who died of a separate brain disease after receiving injections of growth hormone, a study suggests.

An investigation has shown for the first time in humans that Alzheimer's disease may be a transmissible infection which raises questions about the safety of some surgical procedures that could inadvertently pass the brain disorder from one person to another.

Scientists emphasised that the new evidence is still preliminary and should not stop anyone from having surgery. They have also stressed that it is not possible to transmit Alzheimer's by living with or caring for someone with the disease.

However, the findings of a study into eight people who were given growth hormone injections when they were children have raised the disturbing possibility that Alzheimer's can be transmitted under certain circumstances when infected tissues or surgical instruments are passed between individuals.

Until now, it was thought that Alzheimer's occurred only as a result of inheriting certain genetic mutations, causing the familial version of the disease, or from random "sporadic" events within the brain of elderly people, said Professor John Collinge, head of neurodegenerative diseases at University College London (UCL).

"What we need to consider is that in addition to there being sporadic Alzheimer's disease and inherited or familial Alzheimer's disease, there could also be acquired forms of Alzheimer's disease," Professor Collinge said.

"You could have three different ways you have these protein seeds generated in your brain. Either they happen spontaneously, an unlucky event as you age, or you have got a faulty gene, or you've been exposed to a medical accident. That's what we're hypothesising," he said.

"It's important to emphasise that this relates to a very special situation where people have been injected essentially with extracts of human tissue. In no way are we suggesting in any way that Alzheimer's is a contagious disease. You cannot catch Alzheimer's disease by living with or caring for someone with the disease," he added.

The eight adults, aged between 36 and 51, all died of Creutzfeldt-Jakob disease (CJD) after receiving contaminated hormone injections as children. Autopsies on their brains revealed that seven of them harboured the misfolded proteins associated with the early stages of Alzheimer's disease - unheard of in this age group.

They did not, however, find the "tau" protein tangles associated with the later stages of the disease, which means the seven individuals did not have full-blown Alzheimer's, although they may well have developed it had they not died of CJD, Professor Collinge said.

The study, published in the journal Nature, eliminated other possible reasons for the presence of these so-called amyloid-beta (A-beta) proteins and came to the conclusion that they were most likely transmitted as protein "seeds" in the growth-hormone injections - Alzheimer's patients are known to have the A-beta proteins in their brain at least10 years prior to the onset of clinical symptoms

Questions remain about whether these protein seeds could also be transmitted on surgical instruments used in other operations. It is know that the prion proteins behind CJD and Alzheimer's stick to metal surfaces and can survive extreme sterilisation procedures such as steam cleaning and formaldehyde.

There is also the question of whether Alzheimer's disease could be passed in blood transfusions, given that animal experiments have shown this to be possible, with at least one documented instance of CJD being transmitted in a blood donation taken from someone who was incubating the disease but not showing any symptoms.

The seven Alzheimer's risk factors

"It is not clear here with what we are seeing that this is relevant to blood transfusions, and epidemiological studies have been done in the past looking for links between Alzheimer's disease and blood transfusions and they have not shown an association - that's not to say it could never happen," Professor Collinge said.

"Certainly with vCJD, which is the form of CJD associated with mad-cow disease, there is infectivity found in the blood and there has been four documented cases in the UK of vCJD from a blood donor who went on to get vCJD, so it can occur," he said.

"Certainly there are potential risks in dentistry where it is impacting on nervous tissue, such as root-canal treatments and special precautions are taken for that reason. If you are speculating whether a-beta seeds are transmitted at all by surgical instruments one would have to consider whether certain types of dental procedures might be relevant," Professor Collinge said.

"Although it is not cause for alarm that it is in any way contagious, it doesn't mean we shouldn't think about whether there might be accidental routes by which these diseases might be transmitted by certain medical procedures," he added.

In a statement issued afterward, Dr Collinge said: "Our findings relate to the specific circumstance of cadaver-derived human growth hormone injections, a treatment that was discontinued many years ago. It is possible our findings might be relevant to some other medical or surgical procedures, but evaluating what risk, if any, there might be requires much further research. Our current data have no bearing on dental surgery and certainly do not argue that dentistry poses a risk of Alzheimer's disease."

Between 1958 and 1985 some 1,848 people in Britain, mostly children, received growth hormone injections made from tens of thousands of homogenised pituitary glands derived from the brains of human cadavers.

The NHS switched to synthetic growth hormone in 1985 when scientists realised that pituitary-derived hormone could be a route for transmitting CJD. Up to 2000, there were 38 known cases of "iatrogenic" CJD resulting from growth hormone injections in the UK, but this figure is likely to rise further because of the exceptionally long incubation period of the disease.

Of the seven who had the early signs of Alzheimer's, four had severe deposits of amyloid-beta protein, three had moderate deposits and one had traces.

Importantly, they also had protein deposits in the blood vessels to the brain which is also seen in animals that have been infected with human Alzheimer's disease via injection of brain material into their abdomens - a similar transmission route in the eight individuals injected with growth hormone.

Dame Sally Davies, the Government's chief medical officer, has played down the significance of the research saying that it was a small study on only eight samples.

"There is no evidence that Alzheimer's disease can be transmitted in humans, nor is there any evidence that Alzheimer's disease can be transmitted through any medical procedure," Dame Sally said.

"I can reassure people that the NHS has extremely stringent procedures in place to minimise infection risk from surgical equipment, and patients are very well protected," she added.

John Hardy, Professor of Neuroscience at UCL, said: "I think we can be relatively sure that it is possible to transmit amyloid pathology by the injection of human tissues which contain the amyloid of Alzheimer's disease. Does it have implications for blood transfusions? Probably not, but this definitely deserves systematic epidemiological investigation. Does it suggest Alzheimer's disease is infectious through contact? Almost certainly not."

Doug Brown, director of research at Alzheimer's Society, said: "While these findings are interesting and warrant further investigation, there are too many unknowns in this small, observational study of eight brains to draw any conclusions about whether Alzheimer's disease can be transmitted this way.

"Injections of growth hormone taken from human brains were stopped in the 1980s. There remains absolutely no evidence that Alzheimer's disease is contagious or can be transmitted from person to person via any current medical procedures."

What is a prion?

Alzheimer's disease is now considered a "prion disease". Prions, short of proteinaceous infectious particles, are misfolded proteins that carry the ability to trigger further proteins to misfold, leading to debilitating brain disorders, such as CJD and kuru in humans, BSE in cattle and scrapie in sheep.

Prions are unique in being an infectious agent without any genes, unlike viruses or bacteria. They are extremely tenacious, sticking to metal surfaces of surgical instruments and surviving the high temperatures and chemical agents that kill off infectious viruses and microbes.

Stanely Prusiner of the University of California coined the word Prion in the early 1980s and his pioneering work on them led to a Nobel prize in 1997.

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Alzheimer's disease 'may be a transmissible infection'

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The "seeds" of Alzheimer's disease may be transmitted from one person to another during certain medical procedures - possibly including blood transfusions and dental treatment - following a study into people who died of a separate brain disease after receiving injections of growth hormone, a study suggests.

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New Research: Immune System Plays a Key Role in the Development of  Alzheimer's Disease 

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New Research: Immune System Plays a Key Role in the Development of  Alzheimer's Disease 

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Researchers of Harvard medical school released a study which views Alzheimer's disease to be, "triggered by a normal immune response gone astray or into over-drive in response to bacteria or other pathogens..." Moreover, the view and finding of the researchers suggests brains, especially of older people, may overreact to pathogens including herpes, chlamydia, and bacteria responsible for Lyme disease, leading to Alzheimer's disease.

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CLOSE

Researchers at Harvard this week offered a new theory of Alzheimer's Disease that - if true - would upend our understanding of the disease and suggest new routes for treatment and prevention.

The researchers think that the immune system may play a key role in the development of Alzheimer's, which slowly robs people of their memory and is eventually fatal.

A protein called beta amyloid, long considered the bad actor in Alzheimer's, actually plays a positive role in fighting off bacteria and fungus in mice, worms and cells, the researchers showed in a new paper in Science Translational Medicine.

Assuming that's also true in people, it suggests that getting rid of amyloid, as some drug trials have tried, could be dangerous, and approaches that stimulate the immune system could be safer and more effective.

In this view, Alzheimer's would be triggered by a normal immune response gone astray or into over-drive in response to bacteria or other pathogens, according to the paper's authors, Rudy Tanzi and Robert Moir, both of Harvard Medical School and Massachusetts General Hospital.

Amyloid "lights the fire," said Tanzi, whose work has been supported by a grant from the Cure Alzheimer's Fund. "We think it's meant to be beneficial, but it can turn against you and cause problems."

That doesn't mean Alzheimer's is contagious, but that some people's brains may over-react to or get overwhelmed by a variety of pathogens, including chlamydia, herpes and the bacteria that causes Lyme disease, Tanzi said. It's possible that younger people's brains can handle such issues, but some older ones can't.

Alzheimer's is believed to begin in late middle age, though the symptoms may not be evident until a decade or more later.

This view also adds weight to the idea that adequate exercise, high quality sleep, healthy diet and other lifestyle factors like treating gum disease can help prevent Alzheimer's, said Tanzi, who co-wrote a book, Super Genes, with Deepak Chopra, laying out the ways that healthy living can help people avoid Alzheimer's.

James Hendrix, director of global science initiatives with the Alzheimer's Association, agreed that lifestyle factors could make a crucial difference. "If our brain is functioning properly and working the way it should, it will be able to fight off infection," he said.

Vaccines or drugs that reduce inflammation might also be helpful, though the timing of such approaches will be key, said Gary Small, a professor of psychiatry and aging at UCLA's Semel Institute. His own research has shown that healthy people who took anti-inflammatory drugs for 18 months had better brain function than those who took a placebo. But if they started the drugs after Alzheimer's began developing, it could accelerate the disease. "There's a tipping point," he said, but no one yet knows where that is.

Several scientists praised the new paper Thursday and encouraged researchers to continue the study.

"I think it's a very elegant theory," said Ashley Bush, a professor of neuroscience at the University of Melbourne in Australia.

The work is far from conclusive, however, and the ideas in the paper are not entirely new, Bruce Kagan, a professor of clinical psychiatry at UCLA, said via e-mail. "We 'cured' Alzheimers in mice over a decade ago, but none of these drugs work in humans."

Moir said he came up with this new theory when looking at an immune protein called LL-37 that acts like amyloid. In moderation, LL-37 is essential for keeping the brain healthy, but an excess of the protein has been linked to ailments from heart disease to rheumatoid arthritis.

Alzheimer's researchers had always considered amyloid to be "junk," involved only in destructive activities, but Moir said he thought amyloid must also have a positive role, because animals have had it for 400 million years.

In the mice, worms and cells the team tested, amyloid helped kill pathogens by surrounding them and caging them in. Such clumps of amyloid have long considered the hallmark of Alzheimer's Disease.

Read or Share this story: http://usat.ly/1THTXLV

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Harvard researchers unveil new Alzheimer's theory

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CLOSE Researchers at Harvard this week offered a new theory of Alzheimer's Disease that - if true - would upend our understanding of the disease and suggest new routes for treatment and prevention. The researchers think that the immune system may play a key role in the development of Alzheimer's, which slowly robs people of their memory and is eventually fatal.

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by Michael Keyes