New skin test detects prion infection before symptoms appear

Prions can infect both humans and animals, causing Creutzfeldt-Jakob disease (CJD) in humans, mad cow disease in cattle, and chronic wasting disease in elk and deer. The infectious, misfolded protein particles often go undetected as they destroy brain tissue, causing memory loss, mobility issues, and ultimately death. Preclinical detection of prions has proven difficult, but new research suggests skin samples hold early signs of prion disease that precede neurologic symptoms. 

"Currently a definitive diagnosis of Creutzfeldt-Jakob disease is dependent on the examination of diseased brain tissue obtained at biopsy or autopsy. It has been impossible to detect at the early preclinical stage," said an associate professor of pathology.

In a ground-breaking study, an international team of researchers successfully used two methods to detect prions in skin samples collected from inoculated rodents. The study provides the first proof-of-concept evidence that readily accessible skin samples could be used to detect prion disease early—before clinical symptoms appear.

In the new study, the researchers successfully detected prions in rodent skin samples as early as two weeks post-infection. They also detected prions in the skin of uninoculated rodents that were housed alongside inoculated cage mates, demonstrating that prion transmission can occur between cohabitating rodents.

Prions were detected in skin samples from the inoculated rodents before they showed any clinical signs of prion disease. The researchers first inoculated the brains of hamsters and humanized transgenic mice with rodent or human prion samples, respectively. Then, they collected skin and brain samples at different time points, and used two different methods to detect disease-associated prion proteins in the tissues. In both hamsters and mice, the researchers detected prions in skin before they could be detected in brain tissue. The researchers concluded that skin prions could serve as a useful biomarker for preclinical diagnosis of prion diseases.

The study compared two highly-sensitive prion detection methods: RT-QuIC (real-time quaking-induced conversion) and sPMCA (serial protein misfolding cyclic amplification). "Both assays were able to efficiently amplify trace amounts of disease-associated prion protein found in the skin tissues of infected animals," said the study's first author. The tests use prions in tissue samples as a template and either normal brain tissue or synthetic prion protein as "building blocks" to dramatically amplify minute amounts of prions to detectable levels.

One of the methods, RT-QuIC, has been used to detect prion particles in symptomatic CJD patients. However, it normally requires invasive cerebrospinal fluid (CSF) sampling that may be contraindicated for certain patients. Additionally, "The CSF-based prion test results could be uncertain in some cases and not all CSF specimens from patients with prion disease are RT-QuIC positive," said an associate professor of pathology. "Although skin samples may not replace CSF in routine RT-QuIC-based prion disease diagnosis, they may be helpful when prion disease is suspected but CSF is either unavailable or RT-QuIC-negative."

The study results build upon previous work by the researchers showing that autopsy skin samples from human prion disease patients exhibit prion seeding and infectivity. The next step will be to develop and validate the skin prion tests for clinical use.

Said the researcher, "Since the skin is readily accessible and skin biopsy is minimally invasive, detection of skin prions will be very useful for monitoring disease progression and assessing therapeutic efficacy during clinical trials or treatments when prion therapy becomes available in the future."

 The researchers were recently awarded a $2.9 million grant to validate the test methods using human skin samples. They will determine if skin prions could serve as a diagnostic biomarker for CJD or a source of prion transmission.

The researchers believe the methods may also be adapted for diagnosis of other diseases involving misfolded proteins. "Sensitive, minimally invasive detection of various misfolded proteins in skin, such as tau in Alzheimer's disease and alpha-synuclein in Parkinson's disease, could be highly valuable for disease diagnosis and monitoring of disease progression and efficacy of treatments," the researcher said. "It's possible that the skin will ultimately serve as a mirror for us to monitor these misfolded proteins that accumulate and damage the brain in patients with these conditions." 
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New compound shows promise in treatment of Alzheimer’s

Some researchers have identified a drinkable cocktail of designer molecules that interferes with a crucial first step of Alzheimer’s and even restores memories in mice.

The binding of amyloid beta peptides to prion proteins triggers a cascade of devasting events in the progression of Alzheimer’s — accumulation of plaques, a destructive immune system response, and damage to synapses.

“We wanted to find molecules that might have a therapeutic effect on this network,” said senior author.

Researchers screened tens of thousands of compounds looking for molecules that might interfere with the damaging prion protein interaction with amyloid beta. They found that an old antibiotic looked like a promising candidate but was only active after decomposing to form a polymer. Related small polymers retained the benefit and also managed to pass through the blood-brain barrier.

They then dissolved the optimized polymeric compound and fed it to mice engineered to have a condition that mimics Alzheimer’s. They found that synapses in the brains were repaired and mice recovered lost memory.

A collaborating team  reported a positive response when they delivered the same cocktail to cells modeled to have Creutzfeldt-Jakob Disease, a devasting neurological condition caused by infection with misfolded prion protein.

The next step is to verify the compounds aren’t toxic in preparation for translation to clinical trials for Alzheimer’s disease.

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The Comprehensive Guide to Alzheimer's Disease

Alzheimer’s disease and dementia are two terms that are often used interchangeably by people, since there’s a common misconception that they both refer to the same condition. However, Alzheimer’s disease is actually just one of the many paths that can lead to dementia.
This is because dementia is merely an umbrella term for a group of symptoms that affect a sufferer’s thought processes and memory. When a person is diagnosed with dementia, they are simply being told that they are suffering from a particular set of symptoms. The next step would then be to work out exactly what causes these symptoms to appear in the first place.
The most common reason for the onset of dementia is, in fact, Alzheimer’s disease, since it has been estimated to be responsible for as many as 70% of dementia cases. However, there are many other causes of dementia, including Huntington's disease, Parkinson's disease, Creutzfeldt-Jakob disease, and Wernicke-Korsakoff syndrome.
Another key difference is that, in certain cases, dementia can be a temporary and reversible condition, while Alzheimer’s disease has been found to be a permanent condition, which only ends up getting worse, as time goes by.

The 3 Main Types of Alzheimer’s Disease

Nearly everyone who suffers from Alzheimer’s disease will eventually begin to experience the same symptoms, including confusion,memory loss trouble with once-familiar tasks, and difficulty in making decisions. However, there are 3 main types of Alzheimer’s disease, and their differences lie in the way that they are contracted:
1. Late-Onset Alzheimer’s
By far the most common form of the disease, at around 95% of all cases, Late-Onset Alzheimer’s is the kind that occurs in people over the age of 65. It may or may not be genetically-linked, since researchers have yet to find a particular gene that causes it, despite their suspicions.
2. Early-Onset Alzheimer’s
This kind of Alzheimer’s is a lot less common, and only accounts for around 5% of all cases. It occurs in people who are under the age of 65, typically in their 40s or 50s, and people who suffer from Down syndrome  have a higher risk of getting it. Scientists have found that early-onset Alzheimer’s has an even greater effect on the brain than its late-onset counterpart, and have linked its formation to a DNA defect contained within chromosome 14. A muscle twitch known as myoclonus is also more common for sufferers of early-onset Alzheimer’s.
3. Familial Alzheimer's Disease (FAD)
This is a rare form of Alzheimer’s that is 100% genetic, which accounts for less than 1% of all Alzheimer’s cases. In affected families, members of at least two generations have typically had this kind of Alzheimer’s, and many cases of early-onset Alzheimer’s are actually linked to FAD.

The Signs & Symptoms of Alzheimer’s Disease

Alzheimer’s disease is a condition that gradually gets worse over time, and that’s why its symptoms are often split into 3 sections: early, middle, and severe stages.
In the early stages of Alzheimer's a person may:
• Find it hard to remember things
• Ask the same questions repeatedly
• Get lost in familiar places
• Lose things or place them in unusual places
• Have trouble handling money and paying bills
• Take longer than they normally would to finish daily tasks
Once Alzheimer's has progressed to the middle stages, the symptoms, particularly memory loss and confusion, grow worse. Other symptoms include:
• Difficulty learning new things and coping with new situations
• Trouble carrying out tasks that involve many steps, such as getting dressed
• Impulsive behavior
• Forgetting the names of common things
• Hallucinations, delusions or paranoia
• Problems recognizing family and friends
• Wandering away from home
 
Once Alzheimer's has progressed to the more severe stages, symptoms include:
• Total lack of communication
• Spending a lot more time asleep
• Weight loss
• Trouble swallowing
• Incontinence
• Complete dependence

The Science Behind Alzheimer’s Disease

Due to the highly complex nature of Alzheimer’s disease, scientists around the world are still not completely sure what causes it, and how it works. However, many years of research have led us to understand a number of key points. Specifically, we know that Alzheimer’s causes certain brain cells to lose their functions and die, and this is what causes memory loss. A process called atrophy (shrinking of the brain) also takes place, which causes a harmful loss of brain volume.
This loss of brain function is believed to be due to the interactions of two types of proteins, known as amyloid and tau, which have been found to block communication between brain neurons. Amyloid has been observed accumulating into plaque-like clusters, while tau has a tendency to build up inside dying cells in what researchers call ‘neurofibrillary tangles’.
Other researchers also believe that chronic inflammation in the brain may also play a role in the onset and development of Alzheimer’s. Inflammation often occurs as a part of the human body’s defense system, and it aids white blood cells in destroying toxins and waste products. However, scientists have found that certain waste products, such as amyloid plaque and tau tangles, are not being eliminated by Alzheimer’s patients' brains, causing their brain cells to remain permanently inflamed, which ultimately leads to the death of many more brain cells each day.

How to Prevent the Onset of Alzheimer’s

While there’s no proven way to guarantee that you’ll never get Alzheimer’s, there are many lifestyle and dietary changes that you can make, which have been found to decrease or delay your chances of contracting this disease later on in life.
Lifestyle Changes

Maintain a healthy average weight
• Never stop learning new skills and expanding your areas of knowledge
• Maintain a varied circle of friends
• Start taking estrogen supplement after menopause (women only)
• Use the internet frequently to stimulate your brain
• Make sure you get a good night's sleep
• Keep your stress levels in check
• Brush your teeth twice a day
• Take care of your eyes
• Try and be as physically active as possible
• Keep diabetes under tight control Dietary Changes
Eat plenty of antioxidant-rich superfoods,  such as black raspberries, elderberries, raisins, and blueberries.
• Avoid eating bad fats
• Treat yourself to cocoa powder and dark chocolate regularly
• Raise your levels of good cholesterol
• Drink 2 to 4 cups of coffee a day
• Drink more black and green tea
• Eat curry or take curcumin(turmeric) pills
• Add a lot more vinegar to your meals
• Take 500 to 1000mcg of vitamin B12 daily
• Drink a glass of wine each day
• Start following a brain-boosting Mediterranean diet

Drugs to Help Manage the Symptoms

Even though there’s still no cure for Alzheimer’s disease, there are two specific types of medication that can aid in managing the disease’s main symptoms – cholinesterase inhibitors and memantine. Both of these drugs have been approved for use by the FDA to treat the symptoms of Alzheimer’s disease, and should always be used under a doctor’s supervision.

Cholinesterase inhibitors are usually used to treat the symptoms of mild to moderate Alzheimer’s. They work by boosting the strength of certain nerve cells that the disease typically attacks. While they can’t completely stop or reverse the disease’s destructive process, they can slow it down quite a bit. Common side effects of cholinesterase inhibitors include diarrhea, nausea, and vomiting, all of which can be reduced by taking your medication with food, and by starting low and upping the dose gradually.

The most common types of cholinesterase inhibitors prescribed are:
• Galantamine (Razadyne) for mild to moderate Alzheimer's
• Rivastigmine (Exelon) for mild to moderate Alzheimer's
• Donepezil (Aricept) for all stages of Alzheimer’s

Memantine (Namenda) is usually used to treat the symptoms of severe Alzheimer’s. It works by regulating one of the brain’s most important messenger chemicals – glutamate. Memantine is typically taken in the form of a syrup or pill, and the most common side effects include confusion, agitation, headaches, and dizziness.

If none of the medications above are working on their own, the FDA has also approved the use of donepezil in combination with memantine (Namzaric), which is usually found in capsule form. Common side effects include headaches, diarrhea, nausea, and vomiting.

Coping Tips For Alzheimer’s Sufferers

Being diagnosed with Alzheimer’s disease is always devastating news, but as soon as you get over the initial shock, you need to start finding ways to cope, so that you’ll be able to maximize your independence for the foreseeable future. Here are some tips that will help you better handle your day-to-day tasks, and keep on living a meaningful life:

• Create a strong coping strategy by identifying new challenges, prioritizing them, and creating a solution that works best for you.
• Set realistic goals, and only focus on things that you can do today!
• Develop a daily routine that’s easy to follow.
• Never try and multitask!
• Learn to recognize stress triggers.
• Realize that you have more than one shot at fixing most problems.
• Draw inner strength from family, friends, prayer, pets, hobbies, or anything else that you love!
• Try your best to be independent, but don’t be afraid to ask for help.

Coping Tips For Caregivers

It can be sad to see a relative, loved one or friend deteriorate from the effects of Alzheimer’s, but there are quite a few things that you can do to help make their quality of life a lot better, as well as making your job a little easier. Here are a few things you should keep in mind as a caregiver:
• Don’t even think about trying to argue with an Alzheimer’s sufferer – you will get nowhere.
• Ignoring the symptoms won’t make them go away.
• Be aware that too much medication can actually cause further memory loss, so always check with your doctor which ones are really necessary.
• Always listen to what they have to say, even if it makes little sense to you.
• It’s never too late to work on improving their brain health.
• Share your struggles and be open to receiving help.
• Remember to give yourself a break every once in a while.
• Don’t forget to prioritize!
• Remember that 20 minutes for you can feel like a whole day for them.
• Have difficult conversations about medical/legal issues early on, so that you can ensure that you will honor their wishes later on.

The Most Promising Scientific Studies So Far

With every year that passes, members of the scientific community keeps gaining more and more knowledge about how Alzheimer’s disease works, and are constantly searching for new ways to prevent it, slow down its progression, and ultimately to cure it. While they haven’t fully succeeded in finding a complete cure yet, the future looks bright, and below we’ve listed some of the most promising studies that have been carried out so far:
1. How Vitamin E levels affect Alzheimer's
2. The link between bacteria and Alzheimer's disease
3.Scientists successfully manage to reverse Alzheimer's in mice
4.Scientists manage to spot Alzheimer's 15 years in advance
5. Non-invasive ultrasound clears the brain of amyloid plaque.
6. Deep brain stimulation to keep Alzheimer's at bay
7. Blood thinning drugs may prevent dementia 

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Brain-maiming protein may have spread via surgery

A dangerous protein that attacks the brain's blood vessels may have infected children via poorly sterilized surgical instruments decades before the onset of harmful bleeding, researchers reported recently.

Investigating a quartet of mysterious cases in Britain of brain lesions caused by amyloid beta deposits in young adult patients, they found that all four had undergone brain surgery as kids, suggesting a causal link.

"It is introduced into children, takes 30 years to develop, and then -- when they are in their 30s -- the blood vessels are completely loaded with amyloid beta, which destroys the vessels," a professor of Neurology and lead author of a study detailing the findings, told the media.

"This is a very well-known phenomenon in the elderly, but it is unknown in young people."

A large-scale review of medical registries -- already in the pipeline -- will be needed to confirm the deadly protein can be spread by dirty surgical instruments, he added.

Amyloid beta is one of the signature proteins of Alzheimer's, but there were no signs of the disease in the cases examined, according to the study published recently.

"We didn't find any significant amount of the pathological tau protein, which is the other hallmark protein of Alzheimer's," the lead author said.

Previous work with lab animals had shown that tiny amounts of amyloid beta can stick to steel wires and transmit the pathology into animals' brains.

In 2015, the researchers uncovered amyloid beta deposits in the brains of people who had been treated as children with growth hormones extracted from human cadavers, another indication the protein can jump from one person to another.

It has also long been known that the brain-wasting protein that causes Creutzfeldt-Jakob disease, the human variant of "mad cow" sickness, can be passed on via medical procedures, or by eating infected brain matter.

Hospitals sterilize surgical equipment with high-pressure steam and chemicals that kill viruses and bacteria, but the new findings suggest these methods may not always be adequate.

'Just sterile dirt'

"What we didn't know at the time is that proteins can still be transmitted," said the researcher, who worked as a neurosurgeon for several years in the early 1990s.

He recalled one surgeon at work holding up a stainless steel instrument that had residue from a previous operation.

"'Don't worry,' the nurse in charge of sterilisation said through her mask, 'it's just sterile dirt'."

Hygiene standards are more stringent now, but the capacity of brain-attacking proteins to withstand sterilization is still unknown.

The incidence of infection during surgery with amyloid beta may be far higher than suspected, the researcher said.

But if the protein is transmitted into an adult and doesn't show up until late in life, it then becomes impossible to know whether it comes from the brain operation or the natural ageing process.

Unlike Creutzfeldt-Jakob disease, which causes one death per million people each year, amyloid beta build-up is very common among the elderly, even when there are no signs of dementia.

"So that means that there might a lot more cases of contamination, but that we simply can't tell them apart," the researcher said.

Outside experts said the results were suggestive but needed to be backed up by more research.

"This study provides strong, if circumstantial, evidence for an association between neurosurgery in childhood and the development in late adult life of cerebral amyloid angiopathy (CAA)," said  a clinical psychiatrist, using the clinical name of the disease caused by the protein.

The chief scientific officer at Alzheimer's Research , made a similar assessment, adding: "Any potential link will need to be explored in much larger studies."
The researcher said he has already gotten a green light from ethics watchdogs to comb through neuropathology records.

"We plan to identify those brain biopsies of people 50 or younger who -- for any reason -- had a brain bleed caused by amyloid beta," he explained.

"Then we'll go to the clinical notes to check if they had a surgical procedure in their childhood."

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