Dementia is not a single disease but rather encompasses a diverse array of cognitive disorders that pose unique challenges in diagnosis and treatment. While Alzheimer’s disease accounts for most cases, there are over 200 known types of dementia, each with distinct biological underpinnings. Understanding this complexity is the key to developing more targeted therapies.
Alzheimer’s disease is the most common yet complex type
Alzheimer’s disease, characterised by amyloid plaques and neuroinflammation, is the predominant yet most complex form of dementia, accounting for 60–80% of cases. This progressive disorder impairs memory, thinking, and behaviour, ultimately impacting the ability to perform daily activities.
While the exact causes are still being unravelled, we know Alzheimer’s is associated with the buildup of two abnormal protein fragments in the brain: beta-amyloid plaques and tau tangles. These fragments disrupt communication between nerve cells, causing them to die. The plaques and tangles initially form in brain regions involved in memory but eventually spread to other areas as the disease progresses.
Though some cases are hereditary, most Alzheimer’s is considered sporadic, with risk factors including age, family history, head injury, vascular conditions like hypertension, and lifestyle factors like obesity. Recent research shows hearing loss and social isolation can also significantly increase the risk.
Current Alzheimer’s treatments, like cholinesterase inhibitors, may temporarily improve cognition but do not alter disease progression. However, new approaches like amyloid beta-clearing antibodies show promise in removing toxic proteins early on. Other emerging therapies aim to reduce inflammation and support cell health.
While Alzheimer’s poses significant challenges, continued research into its complex biology offers hope. As we better understand the interplay between genetic, molecular, vascular, and lifestyle factors, more effective therapies can be developed to slow or even halt progression. For patients and families impacted, unravelling Alzheimer’s intricate web remains imperative.
Lewy body dementia – marked by Parkinson’s-like symptoms
Lewy body dementia is characterised by abnormal protein deposits called Lewy bodies forming in brain regions involved in thinking, memory, and movement control. These deposits disrupt chemical signalling, impairing cognition and causing movement symptoms like those seen in Parkinson’s disease.
Lewy body dementia accounts for 10–15% of dementia cases overall. Cognitive symptoms include visuospatial disorientation, difficulty with complex mental activities, and fluctuations in attention/alertness. Parkinson’s-like motor disturbances include tremors, rigid muscles, impaired balance, and slow movement. Recurring visual hallucinations are also common.
Two subtypes of LBD exist: dementia with Lewy bodies, marked by early cognitive decline, and Parkinson’s disease dementia, where motor symptoms precede dementia by a year or more. Despite differences, both involve progressive neurodegeneration and α-synuclein protein buildup.
The underlying causes involve a combination of genetic, environmental, and lifestyle factors that promote α-synuclein aggregation and neuroinflammation. Management focuses on the symptomatic treatment of cognition, movement, and behaviour. Emerging research targets neuroinflammation and protein clearance pathways as potential therapies to slow progression.
Frontotemporal dementia – affecting younger individuals
Frontotemporal dementia (FTD) involves progressive cell degeneration in the brain’s frontal and temporal lobes – areas that control behaviour, personality, and language. Symptoms often emerge between ages 45 and 65, earlier than most dementias.
In FTD, portions of these lobes shrink and lose nerve cells, causing dramatic changes in behaviour and personality. Sufferers may act in socially inappropriate ways, exhibit compulsive behaviours, or show a lack of inhibition or empathy. Language variants also exist, with progressive difficulties in speech production or comprehension.
Around 10% of FTD cases are hereditary, linked to mutations in genes like C9orf72 and GRN that cause abnormal protein clumping. Sporadic forms involve a complex interplay of genetic and environmental factors that cause sustained inflammation and neurodegeneration.
Treatments aim to alleviate symptoms and slow progression, with research targeting known genetic drivers and inflammatory pathways. Early, precise diagnosis is critical, allowing patients to access support services and emerging treatments at the earliest opportunity.
Vascular dementia: the role of cardiovascular health
Vascular dementia develops when brain cells are deprived of vital oxygen and nutrients. This often results from damage to blood vessels, impairing blood flow. Strokes, mini-strokes, and small vessel disease play a major role.
Symptoms vary depending on the location and extent of damage but often include slowed thinking, disorientation, difficulty with planning or organisation, and an unsteady gait. Mood and personality changes may also occur.
Risk factors highlight the close link between vascular and cognitive health. These include hypertension, high cholesterol, diabetes, obesity, atherosclerosis, and a history of stroke or heart disease. Lifestyle factors like smoking and a lack of exercise also raise the risk significantly.
Treatment involves intensively managing underlying conditions through diet, exercise, and medication to prevent further vascular damage. Cognitive decline can often be delayed or minimised through prompt, targeted vascular care. Physical and mental activity are also encouraged.
While incurable, vascular dementia is largely preventable through proactive cardiovascular health measures. This underscores the intricate interplay between mind and body, with broad implications for dementia treatment and prevention.
Mixed dementia is a common yet overlooked type
While dementia types are classified separately, mixed dementia – where abnormalities characteristic of multiple dementias are present – is increasingly recognised as a common occurrence, accounting for up to 45% of cases.
Alzheimer’s and vascular pathology often occur together. Some individuals have hallmarks of several dementia types. Overlapping symptoms like memory loss and functional decline make mixed dementia hard to recognise.
Mixed pathologies likely interact to drive progression, necessitating a more nuanced approach to care. Lifestyle measures like exercise and cognitive training combined with Alzheimer’s medications and vascular disease management offer the best outcomes.
Advances in PET imaging and spinal fluid analysis can identify overlapping pathologies in life, improving diagnosis and allowing tailored treatment. More research is still needed to unravel how different dementias biologically interact to devastate cognition and daily living.
The intricate landscape of dementia, with its myriad forms and overlapping symptoms, poses significant challenges in diagnosis and treatment. Yet, with continued research and a deeper understanding of the underlying biology, there is hope for more targeted and effective therapies in the future. As we unravel the complexities of this condition, the path towards better care and possibly a cure becomes clearer.
Jane Hays is a neuroscience writer who aims to make complex brain science accessible to broad audiences.