How does memory normally work?
To understand Alzheimer's and Dementia, it helps to start with a tiny bit of background on how your brain stores memories.
Your brain contains roughly 86 billion nerve cells, each connecting to thousands of others. Memory works by strengthening the connections between nerve cells that fire together when you experience something. The more times those cells fire together, the stronger the connection, which is why repetition helps you learn.
The part of the brain most involved in forming new memories is called the hippocampus. If you've ever noticed that people with Alzheimer's or Dementia often remember events from decades ago very clearly, while struggling to remember what they had for breakfast, it's because the hippocampus, which processes new memories, is usually one of the first areas affected.
What is cognitive decline?
Cognitive decline is a physical illness that causes real, measurable damage inside the brain. It's not simply 'getting old' or 'becoming forgetful'. And crucially, it's not something the person with the disease has done wrong or could have prevented.
Scientists have found two types of damage that are the hallmarks of Alzheimer's. Both involve proteins, the building blocks that cells use to do almost everything, behaving in ways they shouldn't.
Tau protein
The first type is a sticky substance called amyloid beta. In a healthy brain, amyloid beta is produced, used, and then cleared away. In Alzheimer's, it isn't cleared properly, so it builds up in the spaces between nerve cells and forms hard, sticky clumps called plaques.
What is cognitive decline?
Tau protein
The second type involves a protein called tau, which normally works inside nerve cells as part of the cell's internal skeleton, helping to keep the cell's transport system running smoothly.
In Alzheimer's, tau changes shape and starts to tangle up inside the cell, like wool that's become hopelessly knotted. These tangles choke the cell from the inside out.
The plaques and the tangles together cause nerve cells to lose their connections with each other, then eventually to die. As more and more cells are lost, different abilities decline: first memory, then language, then orientation, then the ability to manage daily life.
when does decline start?
One of the most important things researchers have discovered in the last 20 years is that Alzheimer's doesn't start when you notice the first memory problem. It starts much, much earlier, typically 15 to 20 years before any symptoms appear.
During all those years, amyloid plaques are slowly building up. The brain compensates remarkably well for a long time, rerouting signals and recruiting backup connections.
Symptoms only emerge when the damage has become so widespread that the brain can no longer compensate.
This has big implications for treatment. If we can find the disease while it's still silently developing, before symptoms begin, future treatments have a much better chance of making a real difference.
what does it look like?
Early Alzheimer's and Dementia often looks like repeated questions about recent events, difficulty finding words mid-sentence, getting confused in familiar places, and losing track of dates.
These are frustrating and frightening experiences, and many people are aware that something isn't right long before a diagnosis is made.
As the disease progresses, more abilities are affected. Language, spatial awareness, and the ability to manage finances or plan tasks may all become difficult. In later stages, people may not recognise family members and may need help with all aspects of daily life.
It's important to say that behind the disease, the person is still there. People with Alzheimer's and Dementia retain their personalities, emotions, and capacity to connect with others for much longer than people often assume.
why do plaques and tangles form?
The clean-up crew stops keeping up
Amyloid beta isn't inherently bad. It's a normal by-product of brain activity. The problem in Alzheimer's is that the brain's clearing systems can't keep pace with production. Think of it like a sink that slowly drains more and more slowly over years, until water eventually starts to overflow.
Your genes play a big role in how well your brain clears amyloid. A variant of a gene called APOE, particularly the version called APOE ε4, makes the brain's clean-up systems significantly less efficient.
People who inherit one copy of this variant have a noticeably higher risk of Alzheimer's; those who inherit two copies have a much higher risk. But having the gene doesn't mean you will develop Alzheimer's. It's one risk factor among many.
The plaques trigger the tangles
Here's where the two types of damage are connected. Scientists believe the build-up of amyloid plaques triggers a chain reaction that causes tau to change shape and start forming tangles inside cells. The plaques light the fuse; the tangles are what actually destroy the cells.
Tau tangles don't spread randomly. They follow a very predictable path through the brain, starting in the memory areas and gradually moving outward to other regions. This is why Alzheimer's so reliably follows the same pattern of decline: memory first, then other abilities later.
The brain's immune system overreacts
The brain has its own immune cells called microglia. When they spot the amyloid plaques, they try to clear them. But in Alzheimer's, this process goes wrong. Instead of quietly cleaning up, microglia become chronically inflamed and start releasing substances that damage surrounding nerve cells and their connections.
This inflammation appears to be a major driver of the disease's progression, which is why anti-inflammatory approaches are a big focus of current research.
current research
Drugs that can actually remove the plaques
For the first time in history, we have drugs that can remove amyloid plaques from the brains of living people.
Two treatments, lecanemab and donanemab, use antibodies (the same type of targeted proteins your immune system makes) to find and clear amyloid plaques.
Clinical trials have shown these drugs can slow the rate of cognitive decline in people in the early stages of Alzheimer's.
They're not a cure, and they carry some risks, but they represent a genuine scientific breakthrough: the first proof that targeting the underlying disease process can make a real difference.
current research
A blood test that can spot Alzheimer's early
Scientists have developed blood tests that can detect early signs of Alzheimer's, including abnormal amyloid and tau proteins, with an accuracy that rivals expensive brain scans. This could eventually make early detection as simple as a routine blood test at your GP surgery.
Lifestyle factors that make a difference
Large studies have found that roughly 40% of Alzheimer's cases may be linked to factors we can actually influence, such as cardiovascular health, physical activity, social engagement, sleep quality, and managing hearing loss. This doesn't mean Alzheimer's is your fault if you develop it, but it does mean there are real steps everyone can take to reduce their risk.