An article written by Tim Webster for a UK magazine
In May 2019, Alzheimer’s Research UK warned that dementia was “the greatest health challenge of our time” Overdramatised? Take a look at these numbers.
Accounting for more than one in ten of all deaths, dementia is the leading cause of death in the UK. According to Alzheimer’s Research UK, the number of people living with dementia in 2024 is estimated to be 982,000, rising to 1.4 million by 2040. The economic impact of dementia is expected to more than double by 2040, rising from £42.5bn in 2024 to over £90bn in 2040. On an individual basis, someone with mild dementia costs the UK £28,777 a year, while for someone with a severe form of the disease, the figure is £80,499. One in two of us will be affected by dementia in our lifetime, either by caring for someone with the condition, developing it ourselves, or both.
Dementia is an umbrella term encompassing over 100 subtypes characterised by the progressive loss of brain cells (neurons) resulting in a decline in cognitive function. The exact causes vary by type, but the underlying pathophysiology of dementia typically involves structural and chemical changes which impair memory, language, behaviour and executive function (planning and decision-making). Dementia is not a normal part of ageing.
Plaques and Tangles
Alzheimer’s Disease (AD) is by far the most common form of dementia (60% – 80%). There are two brain proteins that, when they misbehave, are associated with Alzheimer’s: Amyloid Precursor Protein (APP) and Tau.
Amyloid precursor protein (APP) is a normal brain protein that helps with cell growth and repair. Enzymes break it down into smaller fragments as part of the brain’s maintenance and communication processes. This can follow two main pathways. The normal path produces harmless fragments; the abnormal path produces amyloid-beta (Aβ) fragments, which, if not cleared up effectively, can clump together to form amyloid plaques. These plaques disrupt communication between cells, trigger inflammation, and contribute to the death of neurons, leading to memory loss, confusion and cognitive decline.
Tau helps maintain the shape of neurons and transports essential materials within brain cells. In Alzheimer’s, tau clumps together inside neurons to form twisted fibres known as tangles. These tangles disrupt the cells’ internal transport system, impair communication, and eventually lead to cell death.
Plaques and tangles are a defining hallmark of Alzheimer’s and a focus of treatment research.
Other Forms
Vascular dementia is the second most common type of dementia. Causes include strokes, mini-strokes (TIAs), high blood pressure, atherosclerosis, diabetes and heart disease. In the case of vascular dementia, neuronal death is caused by impaired blood flow, depriving the brain of oxygen.
Mixed dementia is a condition where a person has two or more types of dementia happening at once. The most common combination is Alzheimer’s and vascular dementia. Because many symptoms overlap, mixed dementia can be challenging to diagnose.
In Lewy body dementia (LBD), neuronal death is caused by abnormal deposits of the alpha-synuclein protein, called Lewy bodies. In addition to cognitive impairments, these deposits can lead to Parkinsonian symptoms, including tremor, bradykinesia (slow, small movements), rigidity, hallucinations and sleep disturbances.
Frontotemporal dementia (FTD) results from neuronal damage to the frontal and temporal lobes of the brain, caused by abnormal protein buildup. FTD typically occurs at a younger age than other dementias, often between 45 and 65.
Early-onset refers to dementia diagnosed before the age of 65. It affects approximately 70,800 people in the UK. But according to Dr Hilda Hayo, Chief Admiral Nurse and Chief Executive at Dementia UK, this may be larger: “We know that young onset dementia is poorly recognised and misdiagnosed, which leads to delays in accessing crucial support, she says. “Worryingly, the figure of 70,800 adults who are estimated to be living with the condition in the UK may just be the tip of the iceberg.”
Cognitive Decline
Many of us of a certain age have asked ourselves if our increasing forgetfulness is a precursor to dementia. The broad answer is, probably not. Roughly 40% of people over the age of 65 will experience normal age-related memory loss (I’d have put that number much higher from personal experience), which is characterised by things like occasionally forgetting names, misplacing items, struggling to find the right word in conversation or needing more time to learn new things, all [crucially] while still functioning independently.
Between normal age-related memory changes and dementia sits an intermediate stage called mild cognitive impairment (MCI). MCI involves a more noticeable decline in cognitive abilities, particularly memory, but is still not severe enough to interfere with daily life. About 30% to 50% of people with MCI develop dementia within 5 years.
Progression
Depending on which parts of the brain are affected, different types of dementia tend to have particular symptoms in the early stages. For example, memory loss is common in early-stage Alzheimer’s but is uncommon in early-stage FTD. As damage spreads to more brain areas, symptoms tend to converge. In general terms, dementia progresses through three stages.
Early-stage (mild) dementia is the phase after MCI where symptoms begin to interfere with daily life, though people can still function relatively independently. People with early-stage dementia can often recall childhood events but forget what they had for breakfast. In [very] simple terms, this is because the hippocampus, which creates and stores new memories, is one of the first areas damaged by dementia, which means the breakfast memory doesn’t get formed in the first place. Long-term memories, on the other hand, depend more on other areas of the brain, like the cerebral cortex, that are preserved in the early stages of the disease, which accounts for the childhood recall.
Middle-stage (moderate) dementia is when memory and thinking problems become more obvious and begin to significantly affect daily life. Recognising family and friends and absorbing new information gets harder, and repeating the same question over and over becomes more common. Problems finding the right word and forgetting what is being said mid-sentence can become an issue. Apathy, depression and anxiety are often present, and delusions and paranoia become more common. Independence declines, and supervision is often needed.
The late-stage (advanced) is when symptoms are most severe. Widespread brain damage affects all major functions – cognitive, emotional and physical. The body gradually loses its ability to function normally. There is an increased vulnerability to infections, like pneumonia, and emotional expression may be limited. At this stage, the focus shifts to palliative care.
Genetics
The increasing prevalence of the disease means that many of us have relatives with dementia. This does not mean we will develop it too. While some rare forms of dementia are strongly genetic, most are influenced by multiple factors, including genes and lifestyle. Specific genes, like APOE-e4, are known to increase the risk of developing Alzheimer’s, but they don’t guarantee it. Other risk factors, such as how active we have kept our brains, whether or not we have had a head injury, the state of the blood supply to our brain, whether we smoke, and high cholesterol levels (especially in midlife), are associated with a buildup of the amyloid plaques, which underpin Alzheimer’s.
Behavioural Issues
The more common behavioural challenges associated with dementia include repetition, time shifting, disinhibition and sundowning.
Repetition can be verbal, such as asking the same question repeatedly, or physical, like constantly rubbing their hands. The person often isn’t aware of it and can’t easily control it.
Time-shifting refers to a condition where someone believes they are living in an earlier period of their life. This can manifest as a struggle to remember recent events, a focus on memories, or the inability to recognise familiar people or places. This happens because short-term memory fades, while older memories often remain clearer. The brain fills in gaps in understanding with familiar experiences.
Disinhibition may involve rude remarks, impulsive behaviour, sexual inappropriateness, or aggression. This happens because dementia – especially forms like frontotemporal dementia – affects the brain’s frontal lobes, which help control judgement, impulses, and social behaviour.
Sundowning refers to a rise in confusion, anxiety, agitation, or restlessness that can occur in people with dementia during the late afternoon or evening hours.
Diagnosing
According to Alzheimer’s Research UK, 65.5% of people aged 65 or over in England who are estimated to have dementia had a recorded diagnosis of dementia on 30th April 2025.
Diagnosing dementia involves a careful assessment of a person’s memory, thinking, behaviour and daily functioning. There is no single test for dementia, so doctors use a combination of methods. These may include medical history, physical exams, cognitive tests, blood tests, and brain scans like CT or MRI. It’s also important to rule out other causes, such as depression, medication side effects or vitamin deficiencies. In some cases, referral to a specialist, like a neurologist, may be needed. An early and accurate diagnosis helps with planning, treatment and support.
Treatment
There are a number of dementia medications available in the UK, which can help to manage the symptoms, but they are not disease-modifying. These include cholinesterase inhibitors – donepezil (Aricept), rivastigmine (Exelon) and galantamine (Reminyl) – which are largely prescribed for mild dementia, and Memantine (Ebixa or Axura) which is prescribed to people with moderate or severe Alzheimer’s.
The first drugs shown to slow down the disease, lecanemab and donanemab, both target amyloid beta. They were approved for early Alzheimer’s disease (mild cognitive impairment to mild dementia) by the UK’s Medicines and Healthcare products Regulatory Agency (MHRA) in August 2024. Despite MHRA approval, neither drug is currently available on the NHS due to NICE not approving them on cost-effectiveness grounds, which are estimated at an annual cost of £20,000–£25,000 per patient, plus extra costs for infusions and monitoring, and the intensive MRI/PET/hospitalisation infrastructure needed.
Research
According to the Dementia Research Institute, promising areas of research include the way that specialist immune cells in the brain react to amyloid beta and tau proteins; how proteins in the brain are processed and become abnormal/misfolded, and how abnormal proteins cause connections between neurons (synapses) to break down.
In conclusion, Dementia Research UK says:
“A definitive cure for dementia remains elusive, even though recent clinical trials offer cautious optimism for the Alzheimer form of dementia. One of the difficulties is that the disease process starts long before the person shows symptoms. A decade or more before anyone has noticeable cognitive or behaviour symptoms, the brain changes (amyloid plaques and tangles) can be observed. Advancements in treatments targeting Alzheimer’s disease, particularly in its early stages, have shown some promise in slowing cognitive decline. But there is still a long way to go.”
Sources:
The Alzheimer’s Society
Dementia UK
Alzheimer’s Research UK
Dementia Research Institute
NHS UK
