UNDERSTANDING DEMENTIA: HOW EXERCISE WILL HELP

overview

Dementia is an umbrella term for gradual damage to the brain that results in cognitive impairment. Cognitive impairment includes issues with attention, memory, language, visual and spatial processing, problem solving and executive function. Dementia can eventually lead to emotional, behavioural and speech difficulties as well. Dementia is diagnosed when the cognitive impairments and other symptoms of the patient are severe enough to impact daily living and functioning. It is the 2nd leading cause of death in Australia with more women affected than men and the number of cases ( currently 459,000) expected to double over the next 30 years [1]. In 2018 the cost of dementia was estimated to be $15 billion! The most common types of dementia are Alzheimer’s disease, Vascular dementia, Lewy Bodies dementia and Frontotemporal dementia, which I will discuss briefly. Other forms of dementia include HIV related dementia (HAND), Normal Pressure Hydrocephalus (NPH), Corticobasal Degeneration, Motor Neuron disease and Parkinson’s Disease dementia. A person can have more than one type of dementia at the same time. The risk of getting dementia increases with age as about 1 in 10 people over 65 have dementia [1], although it is possible to get dementia younger than 65 years of age and this is termed ‘Young Onset of Dementia’.

Alzheimer’s Disease (AD):

Accounts for up to 70% of dementia cases. AD usually starts slowly and gradually progresses over time [1]. The cause of Alzheimer’s is poorly understood, but it is generally believed that a combination of genetic, environmental and lifestyle factors affect the brain overtime [2]. Clinically, AD presents initially as difficulty with short term memory, then long term memory and progresses to mood swings, language problems, apraxia (difficulty sequencing and understanding motor commands) cognitive and functional decline until death. Pharmaceutical treatment only offers symptom relief for 6-12 months, but will not prevent or reverse the damage [3]. AD is typically characterised by a pattern of neuronal loss starting in the hippocampus (memory regions) and progressing to widespread frontal and parietal cortex degeneration (language, reasoning and social behavior) [3].

Alzheimer’s core neuropathologic findings include amyloid plaques, tau proteins, leading to synaptic deterioration and eventually neuronal death [4]. It is hypothesised that extracellular amyloid plaques interfere with synaptic activity and results in a cascade dysfunction between neuronal communication and eventually death. However, there is evidence that amyloid plaques are not the primary cause of AD as amyloid plaque burden in cognitively normal adults [4]. Tau protein’s are essential for neuronal growth, however in AD, abnormal chemical changes cause tau protein to detach from microtubles (which guide molecules and nutrients within neurons) and stick to other tau proteins [5]. This causes them to aggregate into neurofibrillary tangles (NFT) within the neurons of the temporal lobe, parietotemporal and frontal lobe. NFT then act to block the synaptic communication between neurons and eventually the neurons die. The density of the Tau NFT within in neurons correlates to the symptom severity of AD. People with AD also present with vascular issues due to amyloid plaques building up in brain arteries as well, which further reduces blood flow and nutrients to the brain [5].

Vascular Dementia (VD):

Accounts for about 20% of cases and is the second leading form of dementia after Alzheimer’s disease [6]. Vascular dementia (VD) is caused by chronic reduced blood flow to the brain, usually as a result of stroke or multiple strokes. Small vessel disease and other cerebrovascular diseases such as atherosclerosis and amyloid plaques also contribute to the cause. In fact, the risk of dementia is doubled after a stroke and the same preventative strategies for stroke and cardiovascular disease are the corner stone for VD prevention [6]. Modifiable risk factors account for 25% of VD cases and this is where exercise can be very influential. The symptoms of VD overlap with Alzheimer’s disease and they can both occur together. People with VD tend to decline more rapidly than those with Alzheimer’s. There are different types of VD, with the two most common being [1];

• Multi-Infarct Dementia: This is the most common form and is caused by multiple strokes. Often the symptoms progressing over time. The strokes cause damage to the regions of the brain responsible for learning, memory and language. In addition to cognitive symptoms, they can have severe depression and mood swings. The strokes are often small and silent until the degree of damage manifests as symptoms for diagnosis.

• Binswanger’s Disease (Sub-Cortical VD): Originally thought to be very rare but now thought to be relatively common. It is also associated with stroke related changes, but with small vessels deep within the brain affecting the ‘white matter’. Upon examination, it’s common to see gait disturbances and asymmetry of sensation, movement and reflexes. Symptoms also include lethargy, emotional mood swings and incontinence. Cognitive symptoms include reduced reasoning and thinking skills and mild memory problems. It is caused by high blood pressure and thickening of arteries [1].

Lewy-Bodies Dementia (LBD):

Accounts for about 7.5% of all dementia cases clinically (when Parkinson’s dementia is included) [7]. However, on post-mortem biopsy we find it accounts for about 15-20% of dementia cases [7]. LBD and patient’s with Parkinson’s disease who develop dementia share pathophysiology and clinical characteristics due to their cortical and sub-cortical lewy body pathology. Most patients who develop LBD are over 50 and there is no specific lifestyle factors that increase the risk.

The exact cause of LBD is unknown but we are understanding more about what is happening. A protein called ‘alpha-synuclien’ aggregates and forms clumps of ‘lewy bodies’ inside neurons of the brain areas responsible for memory and movement. These neurons work less effectively and eventually die. An accumulation of lewy bodies results in a loss of neurons that produce the neurotransmitters (chemical messengers) acetylcholine and dopamine. Acetylcholine is important for memory and learning, while dopamine is important for behaviour, emotion, movement and sleep.

There are three cardinal symptoms for LBD which include visual hallucinations, Parkinsonism (tremor, stiffness, shuffled gait, movement difficulties) and fluctuations in mental states (clear one moment, confused and disorientated the next) [1]. Other common symptoms are hallucinations, autonomic dysfunction (i.e. blood pressure, temp regulation), reduced memory, attention and visual-spatial problems and depression. They have a high frequency of falls due to difficulties judging distances. The progression of LBD is usually more rapid.

Fronto-Temporal Dementia (FTD):

FTD is the least frequent of the common types of dementia, it accounts for about 5% of dementia patients. FTD is an umbrella term for a group of rare disorders that cause shrinkage and death of the frontal and temporal lobes of the brain, unlike Alzheimer’s which affects most areas of the brain. The frontal lobe is responsible for mood, social behaviour, personality, logic, language (receptive and expressive), self control and emotion. It is also responsible for voluntary movement. The symptoms of FTD depend on the location of brain damaged. Memory often remains unaffected in FTD [1]. FTD tends to occur at a younger age, beginning between the ages of 40 and 65. Because FTD is relatively a younger diagnosis and the symptoms a largely behavioural and emotional, a lot of patients are diagnosed with psychiatric illness.

Abnormal Build up of Tau protein and Ubiquitin protein within the neurons of the frontal lobe and temporal lobe resulting in disruption of neural communication and eventual death of neurons is seen in FTD [8]. There is a hereditary genetic link with mutations in the ‘MAPT’ gene (responsible for Tau inclusion), the ‘Progranulin’ gene (responsible for Ubiquitin inclusion) as well as may other genes which have been identified [8]. Three main variants of FTD have been identified and depend on which region of the brain are predominantly affected. The variants are [1];

• Behavioural Variant (Frontal Lobe): These patients demonstrate in personality, behaviour, emotional response and habits. Some patients may become very apathetic while others will become disinhibited (act impulsively and not stop themselves from doing or saying inappropriate things). Reduced ability to perform daily activities is an early feature, however memory is usually intact. Other common symptoms include difficulty with reasoning, planning and organisation, change in eating patterns and a decline in self care and hygiene.

• Semantic Variant (Temporal Lobe): The initial symptom is a decline in language abilities, particularly assigning meaning to words, objects and concepts, i.e. substituting similar words for the intended word, such as ‘uncle’ for ‘brother’. They have difficulty finding the right words and names, this is called ‘aphasia’. Grammar and speech production remain intact but the sentences may make no sense while still sounding fluent. They may also have difficulty with facial recognition of people. Most patients will retain non-language ability until very late into the disease. As the disease spreads into the frontal lobe, changes in emotion, empathy and food preferences are common.

• Progressive Non-Fluent Aphasia (PNFA): Within ‘Broca’s’ speech area of the frontal lobe. It’s the least common form of FTD and tends to have a later onset. It is characterised by slow, hesitant and effortful speech. The ability to speak fluently is gradually lost and have a tendency to produce the wrong word. When they say the wrong word, they understand its the wrong word for the intended meaning, where as in the semantic variant they don’t know. Naming and comprehension are not as effected where as spelling and reading are often impaired. Problems with abstract reasoning, memory and behaviour become evident later.

Treatment for FTD is based around managing difficult behaviours, support for carers and and trying to manage other symptoms such as speech or impairments to daily activities.

exercise for dementia

Finally we get to delve into how we can help with exercise and briefly highlight the what the current research shows. I would also like to mention that speech pathology and occupational therapy in this patient group would also be very beneficial.

We know that dementia patients are a higher falls risk, they become less physically active due to a decline in their functional ability and increased social isolation; this is all on top of the cognitive and behavioural decline which is the hallmark of dementia. So I will briefly look at the benefits of aerobic exercise (AE), resistance training (RT) and give the current recommended minimum guidelines for exercise frequency and intensity. I will relating it to dementia as a whole and not each specific type.

Aerobic Exercise

AE is going to be one of the most powerful tools you have in treating dementia. Firstly in treating the risk of secondary comorbidity due to physical inactivity. It is well documented that improving aerobic fitness will reduce the risk of stroke, cardiovascular disease, diabetes, etc and therefore improving the health and well-being of the patient. What about in treating the actual disease? A systematic review in 2018 concluded that AE retained left hippocampal volume when compared to the control group. This showed that AE had a neuroprotective benefit by reducing the age related decrease in hippocampal volume [9]. This is important as the hippocampus is a region of the brain responsible for memory and typically the first region affected in Alzheimer’s. Another Systematic review from 2020 found that physical exercise slows down the cognitive decline and reduces the behavioural symptoms in patients with mild cognitive impairment and dementia [10]. Furthermore, they found that AE at moderate to high intensity with a total training duration greater than 24 hours was superior in eliciting these benefits when compared to all other exercise modalities. A 2019 study found that AE (moderate intensity treadmill, 4 times per week for 30 min, over 12 weeks) improved cerebral blood flow in patients with mild cognitive impairment [11]. During exercise cerebral blood flow increases by 10-30% and AE is also shown to promote the growth of cerebral arteries. This is also extremely important as cerebral blood flow in dementia is compromised and further adds to the neurocognitive decline. Finally, it’s well established that AE enhances neuroplasticity by increasing neurotrophic (BDNF, NT-3, IGF-1, etc) factors that build and repair our nervous system. These benefits are treating dementia at the cellular level and something that current medication can’t do.

Resistance Exercise

Again, the effects of RE are well known in improving a person’s health and well-being. RE improves strength, bone density, functional capacity such as climbing stairs or getting up from a low chair. It will also reduce the risk of secondary morbidities due to physical inactivity. For these reasons alone, we can see how important it is for someone with dementia. However, RE is also powerful in treating the actual disease process. A systematic review from 2019 found that RT induced function changes in the brain, in particular the frontal lobe, which followed with improvement in executive function [12]. This would be particularly useful in patients with frontotemporal dementia. More so, RT lead to lower white matter (conducting part of the neurons) atrophy and lesions [12]. RT is also essential is maintaining brain health and neuroplasticity by inducing release of neurotrophic factors (BDNF) [12].

Other exercise modalities such as balance training are essential for people with dementia to reduce their falls risk. Also mobility and gait retraining would be important, especially as the disease progresses and develops parkinsonian mobility. And of course for neuroplasticity we need to be practising repetitive experiential stimuli in combination with AE and RT programs; i.e. including cognitive exercises focusing on attention, memory, planning, etc in combination with aerobic and resistance exercises will yield the best results. The minimum recommended guidelines for exercise in dementia are [1];

• Aerobic Exercise for 30 min, 5 days per week and moderate intensity

• Resistance Exercise at least 2 times per week, large muscle groups and moderate to high intensity

• Balance Exercise at least 3 times per week or total of 2 hours

Overall, Exercise can significantly slow the course of your disease and improve your quality of life. I hope you have learnt something from this information and it helps direct you to a path of you improving your life. If you would like to learn more or speak to an Exercise Physiologist that specialises in neurological rehabilitation you can reach out to us via our website, Facebook, email or phone. Please click on the ‘contact’ tab for all our information.

[1] http://www.dementia.org.au

[2] http://www.mayoclinic.org/diseases-conditions/alzheimers-disease

[3] M. Brandon. Establishing RNA Binding Proteins as Key Components of Alzheimer’s Disease Pathophysiology. Boston University, 2020.

[4] http://www.cleavlandclinicmeded.com/medicalpubs/diseasemanagement/neurology/alzheimers-disease

[5] http://www.nia.nih.gov/health/what-happens-brain-alzheimers-disease

[6] F. J. Walters et al. Epidemiology of Vascular Dementia. Atherosclerosis, Thrombosis and Vascular Biology, 2019. Vol 39. Pg. 1542-1549

[7] J. P. M. Kane et al. Clinical Prevalence of Lewy Body Dementia. Alzheimer’s Research and Therapy, 2018. Vol 10 (19).

[8] http://www.uptodate.com/contents/frontotemporal-dementia-epidemiology-pathology-and-pathogenesis

[9] J. Firth et al. Effect of Aerobic Exercise on Hippocampal volume in humans: A Systematic Review and Meta-Analysis. NeuroImage, 2018. Vol 166. Pg. 230-238

[10] C. K. Law et al. Physical Exercise Attenuates Cognitive Decline and Reduces Behavioural Problems in People with Mild Cognitive Impairment and Dementia: A Systematic Review. Journal of Physiotherapy, 2020. Vol 66 (1). Pg. 9-18

[11] A. J. Alfini et al. Resting Cerebral Blood Flow After Exercise Training in Mild Cognitive Impairment. Journal of Alzheimer’s Disease, 2019. Vol 67 (2). Pg. 671-684

[12] F. Herold et al. Functional and/or Structural Brain Changes in Response to Resistance Exercises and Resistance Training Lead to Cognitive Improvements - A Systematic Review. European Review of Aging and Physical Activity, 2019. Vol 16 (10)