Alzheimer's Disease vs Lewy Body Dementia: Differences and Similarities

Alzheimer's disease (AD) and Lewy Body Dementia (LBD) are two similar forms of dementia and, therefore, are characterized by similar progressive degeneration of cognitive abilities. Although they have much in common, there are critical distinctions between AD and LBD that are important to understand. This article will primarily consider differences in the symptoms between Alzheimer's Disease and Lewy Body Dementia.
Klara Hatinova

Klara Hatinova

Klara is postgraduate researcher in experimental psychology at the
University of Oxford.

A blue image with text saying "Alzheimer's vs Lewy Body".

Alzheimer's Disease vs Lewy Body Dementia

Alzheimer's disease (AD) and Lewy Body Dementia (LBD) are both a type of dementia, a condition characterized by impaired cognitive abilities. Even though both diseases are a form of dementia, they are not the same. In fact, there exist many different forms of dementia, such as vascular dementia or frontotemporal dementia

To understand the differences between Alzheimer's and LBD, let's begin by comparing their symptoms. We can separate the symptoms to different categories.

Cognitive Symptoms

The primary cognitive symptom of Alzheimer's disease (AD) is memory loss. Memory problems can significantly impact a person's life - simple tasks like keeping appointments or maintaing a personal hygiene can quickly become difficult [1].

Another common symptom of Alzheimer's Disease is Aphasia, which referrs to trouble with speech or writing. Aphasia is quite common in neurodegenerative diseases, and is also a symptom of frontotemporal dementia.

Patients with AD can also experience disorientation, difficulties with problem-solving and decreased judgment, the so-called executive functioning [1].

The cognitive symptoms in Lewy Body Dementia are somewhat similar to those in Alzheimer's. LBD patients also experience memory loss and decreased executive function, but memory problems are usually less prominent than in Alzheimer's disease. This can include reduced concentration, attention, alertness, and wakefulness. These symptoms can vary from day to day [2].

Behavioral Changes

Behavioural changes are frequently seen in both Alzheimer's disease and Lewy Body Dementia patients. In Alzheimer's disease, these changes include mood and personality changes, decreased motivation to pursue personal hygiene, and withdrawal from friends, family, and community [1]. Depression is also common in Alzheimer's disease, occurring in approximately 17% of patients [3, 4].

Similarly, in LBD, changes in behaviour and mood can include depression, anxiety, and apathy, which is a lack of interest in normal daily activities or events [2].

Non-Cognitive Symptoms

Non-cognitive symptoms of Alzheimer's disease include gait and balance disruption, problems with smell and taste, as well as additional psychiatric symptoms, such as suspiciousness, paranoia, delusions, and hallucinations [5, 3].

In LBD, non-cognitive symptoms initially appear as problems with movement and posture, including slowness of movement, walking difficulty, and stiff muscles. These are collectively called Parkinsonian motor symptoms [2]. One of the earliest symptoms of LBD in some people is REM sleep disorder. This is a condition in which people act out their dreams, experience vivid dreams, talk in their sleep, make violent movements, or even fall out of bed [6].

Progression of the Diseases: Alzheimer's Disease vs Lewy Body Dementia

The critical difference between Alzheimer's Disease and Lewy Body Dementia is the progression of symptoms. In Alzheimer's Disease, memory problems are the first to set in, whereas in Lewy Body Dementia, motor and behavioural problems are more prominent. Lewy Body Dementia also tends to progress faster [7].

Causes: Alzheimer's Disease vs Lewy Body Dementia

The exact causes of both Alzheimer's Disease and Lewy Body Dementia are still unknown and likely include a spectrum of modulating factors. Nonetheless, research has identified several risk factors and potential causes.

In Alzheimer's Disease, age is the most significant risk factor, with most people who develop the disease being 65 years of age or older [7, 8].

Protein Abnormalities

Alzheimer's disease is primarily caused by protein abnormalities in the brain, which can cause brain damage. In particular, amyloid and tau protein abnormalities are considered to be the main culprits responsible for the neurodegeneration in Alzheimer's Disease. The amyloid hypothesis, the predominant framework for AD research for over two decades, suggests that the accumulation of beta-amyloid (Aβ) in the brain disrupts neural communication and leads to the death of cells in affected midbrain areas [9].

Lewy Body Dementia, is caused by the build-up of the so-called Lewy's bodies, in parts of the brain that control memory, thinking, and movement, is believed to be a primary cause [2]. These Lewy Bodies are aggregates of misfolded, abnormal proteins that clump together and prevent communication between neurons in the midbrain [10]. Alpha-synuclein and ubiquitin are examples of two proteins that, when misfolded, can be found in Lewy Bodies [11].

Genetics: Alzheimer's vs Lewy Body Dementia

Genetics also play a crucial role in Alzheimer's Disease. Specific gene variants, such as the apolipoprotein E gene, are linked to an increased probability of developing Alzheimer's Disease. Possession of the APOE epsilon 4 variant increases risk four-fold and reduces the age of onset [12]. Mutations of presenilins 1 and 2 and of the APP gene have been identified in families with early-onset AD [8].

Less is known about the genetic causes of Lewy Body Dementia. Some people with Parkinson's Disease, a condition often associated with LBD, have mutations in the gene that encodes alpha-synuclein, called SNCA. At least 30 mutations associated with have been found in the SNCA gene, leading to changes in alpha-synuclein's structure or excess protein production within cells [10].

Environmental Factors

Environmental factors such as bacterial and viral infections, heavy metal ions, diet, sleep, stress, gut microbiota or oral health are also risk factors for Alzheimer's disease [13]. Copper, for instance, has been found to expedite the formation of Aβ plaques, furthering neurodegeneration [14].

In Lewy Body Dementia, the environmental risks of Lewy Body development have been primarily studied in Parkinson's Disease. Manganese, lead, and pesticide exposure have been linked to increased oxidative stress and dysfunction of the mitochondria, increasing vulnerability to neuronal loss in critical areas [15].

Other Factors

Other risk factors for Alzheimer's Disease include a relative with Alzheimer's Disease, previous head trauma, and certain conditions such as diabetes, hypertension, and Down syndrome [16]. Lifestyle factors, such as smoking and cardiovascular disease, have also been linked to an increased risk of AD [8].

One risk factor for developing Lewy Body Dementia is REM sleep disorder, although it is most likely that alpha-synuclein protein aggregates cause both conditions [17].

Treatment: Alzheimer's Disease vs Lewy Body Dementia

Neither Alzheimer's Disease nor Lewy Body Dementia can be cured. However, treatments to manage the symptoms exist. The treatment of both Alzheimer's Disease and Lewy Body Dementia is multifaceted, involving a combination of pharmacological and non-pharmacological approaches. It's important to note that while these treatments can help manage or alleviate symptoms, they do not stop or reverse the progression of the disease.

Pharmacological Treatments for Alzheimer's Disease and Lewy Body Dementia

In the case of Alzheimer's Disease, the mainstay of treatment is cholinesterase inhibitors, including drugs like donepezil, galantamine, and rivastigmine. These enhance cholinergic transmission in the brain, improving cognitive function. The literature discussing these drugs is rich and a topic of extensive research [22, 23, 24, 25, 26, 27, 28, 29, 30, 31].

For Lewy Body Dementia, cholinesterase inhibitors like donepezil and rivastigmine are also commonly used to improve cognitive symptoms and some psychiatric manifestations, including hallucinations [32].

Memantine, a glutamate antagonist, is approved for use in advanced stages of Alzheimer's Disease, can help slow the progression of symptoms in moderate to severe cases [22, 24, 30, 31]. Aducanumab, a monoclonal antibody that targets amyloid-beta, a protein that forms plaques in the brains of Alzheimer's Disease patients, was approved by the FDA in 2021 and is considered a potential disease-modifying therapy [30].

For Lewy Body Dementia, levodopa is often used to alleviate motor symptoms. However, it should be used with caution as it can potentially worsen hallucinations. Antipsychotic treatment, such as clozapine, may be required for hallucinations in Lewy Body Dementia [32].

Non-Pharmacological Treatments for Alzheimer's Disease and Lewy Body Dementia

Non-pharmacological treatments play a significant role in managing both Alzheimer's Disease and Lewy Body Dementia. For Alzheimer's Disease, intense caregiver support is required to manage behavioural symptoms and functional deficits [33]. Lifestyle changes, including dietary modifications and regular physical activity, can help manage symptoms and improve quality of life [30]. Occupational therapy can help patients maintain their independence and daily living skills for as long as possible [22]. Educational programs can provide caregivers with the necessary skills and knowledge to care for someone with AD [22].

For Lewy Body Dementia, physical therapy can help with movement problems, while occupational therapy helps improve everyday activities. Speech therapy can help with swallowing difficulties and trouble speaking loudly and clearly. Mental health counselling can help manage difficult emotions and behaviours, and music, art or dance therapy may reduce anxiety and improve well-being [2].

Experimental Therapies for Alzheimer's Disease and Lewy Body Dementia

There are several experimental therapies currently under investigation for both Alzheimer's Disease and Lewy Body Dementia. For Alzheimer's Disease, these include anti-inflammatory drugs, antioxidants, secretase inhibitors, tau hyperphosphorylation inhibitors, and amyloid-beta immunization [23, 27, 28, 31].

For Lewy Body Dementia, experimental drugs include interpidine (RVT 101) and nelotanserin [33]. Recent trials have shown promising results for zonisamide and neflamapimod, with improvements in Parkinsonian syndrome and cognition, respectively [34]. Many of these drugs have been re-pruposed form related conditions.

To sum up, the treatment of both Alzheimer's Disease and Lewy Body Dementia is multifaceted, involving a combination of pharmacological and non-pharmacological approaches. While there is no cure, these strategies can help manage symptoms and improve the quality of life for patients with these conditions. Research continues to yield promising targets and modifications, so this field is one to watch.

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Klara Hatinova

Klara Hatinova

Klara is a postgraduate researcher in experimental psychology at the University of Oxford. She has worked across a spectrum of hot topics in neuroscience, including her current project measuring reinforcement learning strategies in Parkinson’s disease. Previously, she studied the efficacy of psilocybin as a therapy for critical mental health conditions and examined molecular circadian rhythms of migraine disorders. She completed her undergraduate degree in Neuroscience at the University of Glasgow and participated in a year abroad at the University of California, where she worked on a clinical trial for spinal cord injury.