What’s the difference? is a new editorial product that explains the similarities and differences between commonly confused health and medical terms, and why they matter.

Changes in thinking and memory as we age can occur for a variety of reasons. These changes are not always cause for concern. But when they begin to disrupt daily life, it could indicate the first signs of dementia.

Another term that can crop up when we’re talking about dementia is Alzheimer’s disease, or Alzheimer’s for short.

So what’s the difference?

What is dementia?

Dementia is an umbrella term used to describe a range of syndromes that result in changes in memory, thinking and/or behaviour due to degeneration in the brain.

To meet the criteria for dementia these changes must be sufficiently pronounced to interfere with usual activities and are present in at least two different aspects of thinking or memory.

For example, someone might have trouble remembering to pay bills and become lost in previously familiar areas.

It’s less-well known that dementia can also occur in children. This is due to progressive brain damage associated with more than 100 rare genetic disorders. This can result in similar cognitive changes as we see in adults.

So what’s Alzheimer’s then?

Alzheimer’s is the most common type of dementia, accounting for about 60-80% of cases.

So it’s not surprising many people use the terms dementia and Alzheimer’s interchangeably.

Changes in memory are the most common sign of Alzheimer’s and it’s what the public most often associates with it. For instance, someone with Alzheimer’s may have trouble recalling recent events or keeping track of what day or month it is.

We still don’t know exactly what causes Alzheimer’s. However, we do know it is associated with a build-up in the brain of two types of protein called amyloid-β and tau.

While we all have some amyloid-β, when too much builds up in the brain it clumps together, forming plaques in the spaces between cells. These plaques cause damage (inflammation) to surrounding brain cells and leads to disruption in tau. Tau forms part of the structure of brain cells but in Alzheimer’s tau proteins become “tangled”. This is toxic to the cells, causing them to die. A feedback loop is then thought to occur, triggering production of more amyloid-β and more abnormal tau, perpetuating damage to brain cells.

Alzheimer’s can also occur with other forms of dementia, such as vascular dementia. This combination is the most common example of a mixed dementia.

Vascular dementia

The second most common type of dementia is vascular dementia. This results from disrupted blood flow to the brain.

Because the changes in blood flow can occur throughout the brain, signs of vascular dementia can be more varied than the memory changes typically seen in Alzheimer’s.

For example, vascular dementia may present as general confusion, slowed thinking, or difficulty organising thoughts and actions.

Your risk of vascular dementia is greater if you have heart disease or high blood pressure.

Frontotemporal dementia

Some people may not realise that dementia can also affect behaviour and/or language. We see this in different forms of frontotemporal dementia.

The behavioural variant of frontotemporal dementia is the second most common form (after Alzheimer’s disease) of younger onset dementia (dementia in people under 65).

People living with this may have difficulties in interpreting and appropriately responding to social situations. For example, they may make uncharacteristically rude or offensive comments or invade people’s personal space.

Semantic dementia is also a type of frontotemporal dementia and results in difficulty with understanding the meaning of words and naming everyday objects.

Dementia with Lewy bodies

Dementia with Lewy bodies results from dysregulation of a different type of protein known as α-synuclein. We often see this in people with Parkinson’s disease.

So people with this type of dementia may have altered movement, such as a stooped posture, shuffling walk, and changes in handwriting. Other symptoms include changes in alertness, visual hallucinations and significant disruption to sleep.

Do I have dementia and if so, which type?

If you or someone close to you is concerned, the first thing to do is to speak to your GP. They will likely ask you some questions about your medical history and what changes you have noticed.

Sometimes it might not be clear if you have dementia when you first speak to your doctor. They may suggest you watch for changes or they may refer you to a specialist for further tests.

There is no single test to clearly show if you have dementia, or the type of dementia. A diagnosis comes after multiple tests, including brain scans, tests of memory and thinking, and consideration of how these changes impact your daily life.

Not knowing what is happening can be a challenging time so it is important to speak to someone about how you are feeling or to reach out to support services.

Dementia is diverse

As well as the different forms of dementia, everyone experiences dementia in different ways. For example, the speed dementia progresses varies a lot from person to person. Some people will continue to live well with dementia for some time while others may decline more quickly.

There is still significant stigma surrounding dementia. So by learning more about the various types of dementia and understanding differences in how dementia progresses we can all do our part to create a more dementia-friendly community.

The National Dementia Helpline (1800 100 500) provides information and support for people living with dementia and their carers. To learn more about dementia, you can take this free online course.

Nikki-Anne Wilson, Postdoctoral Research Fellow, Neuroscience Research Australia (NeuRA), UNSW Sydney

This article is republished from The Conversation under a Creative Commons license. Read the original article.

In a world first, we heard last week that US surgeons had transplanted a kidney from a gene-edited pig into a living human. News reports said the procedure was a breakthrough in xenotransplantation – when an organ, cells or tissues are transplanted from one species to another. https://www.youtube.com/embed/cisOFfBPZk0?wmode=transparent&start=0 The world’s first transplant of a gene-edited pig kidney into a live human was announced last week.

Champions of xenotransplantation regard it as the solution to organ shortages across the world. In December 2023, 1,445 people in Australia were on the waiting list for donor kidneys. In the United States, more than 89,000 are waiting for kidneys.

One biotech CEO says gene-edited pigs promise “an unlimited supply of transplantable organs”.

Not, everyone, though, is convinced transplanting animal organs into humans is really the answer to organ shortages, or even if it’s right to use organs from other animals this way.

There are two critical barriers to the procedure’s success: organ rejection and the transmission of animal viruses to recipients.

But in the past decade, a new platform and technique known as CRISPR/Cas9 – often shortened to CRISPR – has promised to mitigate these issues.

What is CRISPR?

CRISPR gene editing takes advantage of a system already found in nature. CRISPR’s “genetic scissors” evolved in bacteria and other microbes to help them fend off viruses. Their cellular machinery allows them to integrate and ultimately destroy viral DNA by cutting it.

In 2012, two teams of scientists discovered how to harness this bacterial immune system. This is made up of repeating arrays of DNA and associated proteins, known as “Cas” (CRISPR-associated) proteins.

When they used a particular Cas protein (Cas9) with a “guide RNA” made up of a singular molecule, they found they could program the CRISPR/Cas9 complex to break and repair DNA at precise locations as they desired. The system could even “knock in” new genes at the repair site.

In 2020, the two scientists leading these teams were awarded a Nobel prize for their work.

In the case of the latest xenotransplantation, CRISPR technology was used to edit 69 genes in the donor pig to inactivate viral genes, “humanise” the pig with human genes, and knock out harmful pig genes. https://www.youtube.com/embed/UKbrwPL3wXE?wmode=transparent&start=0 How does CRISPR work?

A busy time for gene-edited xenotransplantation

While CRISPR editing has brought new hope to the possibility of xenotransplantation, even recent trials show great caution is still warranted.

In 2022 and 2023, two patients with terminal heart diseases, who were ineligible for traditional heart transplants, were granted regulatory permission to receive a gene-edited pig heart. These pig hearts had ten genome edits to make them more suitable for transplanting into humans. However, both patients died within several weeks of the procedures.

Earlier this month, we heard a team of surgeons in China transplanted a gene-edited pig liver into a clinically dead man (with family consent). The liver functioned well up until the ten-day limit of the trial.

How is this latest example different?

The gene-edited pig kidney was transplanted into a relatively young, living, legally competent and consenting adult.

The total number of gene edits edits made to the donor pig is very high. The researchers report making 69 edits to inactivate viral genes, “humanise” the pig with human genes, and to knockout harmful pig genes.

Clearly, the race to transform these organs into viable products for transplantation is ramping up.

From biotech dream to clinical reality

Only a few months ago, CRISPR gene editing made its debut in mainstream medicine.

In November, drug regulators in the United Kingdom and US approved the world’s first CRISPR-based genome-editing therapy for human use – a treatment for life-threatening forms of sickle-cell disease.

The treatment, known as Casgevy, uses CRISPR/Cas-9 to edit the patient’s own blood (bone-marrow) stem cells. By disrupting the unhealthy gene that gives red blood cells their “sickle” shape, the aim is to produce red blood cells with a healthy spherical shape.

Although the treatment uses the patient’s own cells, the same underlying principle applies to recent clinical xenotransplants: unsuitable cellular materials may be edited to make them therapeutically beneficial in the patient.

We’ll be talking more about gene-editing

Medicine and gene technology regulators are increasingly asked to approve new experimental trials using gene editing and CRISPR.

However, neither xenotransplantation nor the therapeutic applications of this technology lead to changes to the genome that can be inherited.

For this to occur, CRISPR edits would need to be applied to the cells at the earliest stages of their life, such as to early-stage embryonic cells in vitro (in the lab).

In Australia, intentionally creating heritable alterations to the human genome is a criminal offence carrying 15 years’ imprisonment.

No jurisdiction in the world has laws that expressly permits heritable human genome editing. However, some countries lack specific regulations about the procedure.

Is this the future?

Even without creating inheritable gene changes, however, xenotransplantation using CRISPR is in its infancy.

For all the promise of the headlines, there is not yet one example of a stable xenotransplantation in a living human lasting beyond seven months.

While authorisation for this recent US transplant has been granted under the so-called “compassionate use” exemption, conventional clinical trials of pig-human xenotransplantation have yet to commence.

But the prospect of such trials would likely require significant improvements in current outcomes to gain regulatory approval in the US or elsewhere.

By the same token, regulatory approval of any “off-the-shelf” xenotransplantation organs, including gene-edited kidneys, would seem some way off.

Christopher Rudge, Law lecturer, University of Sydney

This article is republished from The Conversation under a Creative Commons license. Read the original article.