The Difference Between Dementia and Alzheimer’s

There are 47 million people living with dementia worldwide, according to the World Health Organization. While dementia and Alzheimer’s may be used interchangeably, there are important differences between them. Here’s what you need to know.

Dementia vs. Alzheimer’s

First thing to know: How to tell the difference between dementia vs. Alzheimer’s disease. Dementia is an umbrella term for symptoms like impaired memory and thinking that interferes with daily living; Alzheimer’s disease is a specific type of dementia. Other types of dementia include vascular dementia, dementia with Lewy bodies, front-temporal dementia, Parkinson’s disease, and Huntington’s disease.
“Alzheimer’s is the most common form of dementia—about 60-70 % of the time a patient with dementia has Alzheimer’s,” says a Dr. The reason you hear about Alzheimer’s most often is not only because it is the most common type of dementia, but also because “the science behind Alzheimer’s is the most advanced across all dementias,” Dr. says. These are some of the early signs of Alzheimer's. 

Causes of dementia are vastly different

A medical illness, metabolic issue (like a nutritional or thyroid problem), vascular disease (like a stroke), or, rarely, infectious diseases can affect brain cells, causing dementia. Even Mad Cow Disease, which is very rare, can contribute to dementia, explains the Dr. A condition called depressive “pseudo” dementia is another possible source. As he explains, when levels of the neurotransmitter serotonin run low, you may have trouble paying attention. And when you’re distracted, you have trouble remembering things, which can manifest as dementia.
On the other hand, Alzheimer’s has its own origins. It’s a brain disease marked by deposits of beta-amyloid plaques and proteins called tau that damage cells in brain regions that control functions like thinking, memory, and reasoning. Here are the habits that can increase your risk of dementia.

Multiple factors can be at play

There’s also what’s called mixed dementia, meaning there are multiple conditions that are coming together to cause dementia. “Thirty percent of the time, patients who have Alzheimer’s also have a vascular disease that makes cognitive symptoms worse,” says a Dr. Alzheimer’s and dementia with Lewy bodies (in this disease, clumps of alpha-synuclein proteins develop in the brain) has also been found to occur together.

Symptoms can look very similar

Losing your keys—again—and forgetting where you parked are basic memory problems, so how do you know when it crosses the line to dementia or Alzheimer’s? According to the Alzheimer's Association, in order for a person to be diagnosed with dementia, two of the following must be “significantly impaired”: memory, communication and language, ability to focus and pay attention, reasoning, and judgment, and visual perception. When it comes to Alzheimer’s, the association notes that you may forget new information or find you have to ask family members to remember important facts you should be able to keep track of yourself. (It’s not those little brain blips where you can’t remember the name of your second cousin and then it comes to you later—that’s normal). Research also indicates that difficulty using a map may be one of the earliest warning signs of Alzheimer’s. These are the warning signs of Alzheimer's to watch out for. 

You may be able to prevent Alzheimer’s

“We have the Alzheimer’s Prevention Clinic, and the fact that you can talk about those words together is advanced,” says the Dr. The clinic investigates how lifestyle choices—a healthy diet, exercise, social and mentally stimulating activities, as well as everyday habits, and ample sleep can markedly reduce your risk of Alzheimer’s. In fact, in a study in 2014 published, reducing certain risk factors can decrease risk of Alzheimer’s by 33 percent. The most important ways to prevent Alzheimer’s: Control diabetes and high blood pressure, reduce weight if obese, stay active, treat depression, don’t smoke, and stay in school. A 2017 study adds that staying social (spend time with friends and family members) and managing hearing loss to the list of controllable factors in the prevention of dementia.

Treatment options depend on the type of dementia

There are virtually no FDA-approved therapies for dementia (only one approved drug for Parkinson’s dementia), but there are four medications that target Alzheimer’s, according to a Dr.  And while these drugs don’t stall disease progression (or cure the disease), they can help control symptoms in patients. Patients of Dr. Isaacson’s say these drugs may help for six to nine months, but many stay on them for the long haul because they help with behavioral symptoms such as agitation and aggression. “When you stop the medications, the psychological symptoms get worse,” he says.

As for other types of dementia, lifestyle changes may be the best option. Treatment for vascular dementia relies on doing things that are healthy for your arteries and heart: reducing blood pressure and cholesterol, and controlling diabetes. “Managing other chronic conditions is important. Those are a great way to press the fast-forward button on dementia,” says the Dr.

You can find out if you’re at an increased risk of Alzheimer’s now

If you get evaluated for Alzheimer’s, your doctor can make a diagnosis based on symptoms, a clinical history, and medical tests (to rule out causes like thyroid issues or nutritional deficiencies). Brain imaging tests like a cat scan or MRI can look for beta amylase plaques gunking up brain regions. If you’re worried that you may be developing Alzheimer’s, The researchers have developed a free, short quiz that will suggest, based on name, face, and occupation recognition, whether you need further evaluation for a possible diagnosis of Alzheimer’s. The results correlate with the levels of beta-amyloid in the brain, he explains. 

You don’t have to be scared

Forgetting how to work the thermostat in your home, being afraid to leave your neighborhood out of fear you might not get home, or misplacing your belongings so often that it hurts your ability to get out the door can all be particularly worrisome—especially if a loved one expresses their concern. If you’re concerned, see your doctor, says the Dr. “Get educated, get informed, get evaluated,” he says, adding “the earlier the diagnosis, the earlier you can be treated. And the earlier you’re treated, the better you’ll do.

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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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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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