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4.1. Alzheimer's Disease
Defining ‘Dementia’ and ‘Alzheimer’s Disease’
Dementia is a syndrome (i.e. a set of symptoms that normally occur together) that is associated with cognitive decline, i.e. thinking problems. The symptoms are caused by progressive damage to particular areas of the brain. The main symptoms are:
Alzheimer’s disease (AD), vascular dementia, dementia with Lewy bodies and frontotemporal dementia are all examples of neurodegenerative diseases that have dementia as their main symptom/syndrome. These neurodegenerative diseases are differentiated from each other by how the disease processes affect brain tissue. Let’s take a look at the development of Alzheimer’s disease below.
- Memory loss (especially of short term, day-to-day memories);
- Decrease in mental agility (for example, of concentration and planning);
- Language problems (holding conversations and remembering certain words become more difficult);
- Orientation (to date, place and time);
- Personality changes, such as increased apathy, anxiety and frustration;
- Behavioural changes, such as becoming less social and performing certain activities over and over again, e.g. pacing up and down;
Alzheimer’s disease (AD), vascular dementia, dementia with Lewy bodies and frontotemporal dementia are all examples of neurodegenerative diseases that have dementia as their main symptom/syndrome. These neurodegenerative diseases are differentiated from each other by how the disease processes affect brain tissue. Let’s take a look at the development of Alzheimer’s disease below.
Biological Processes Underlying Alzheimer’s Disease
Alzheimer’s disease is thought to begin with insulin resistance in the brain, so it is sometimes called ‘diabetes of the brain’. As such, Alzheimer’s disease is considered to be a neurodegenerative and metabolic disease.
Research suggests that insulin resistance facilitates the aggregation of a protein called amyloid-beta in the hippocampus. These aggregations, or collections, of protein build up over time, forming amyloid-beta plaques. These plaques stimulate an immune response from microglia in the brain, which begins a cascade of cellular activity that damages neurons and prevents them from functioning normally. The neurons in the hippocampus eventually begin to die and, because the hippocampus is essential for forming memories, memory problems and dementia are common symptoms. Plaques also build up in the cerebral cortex and so neuronal death occurs there too. The neurons that are most likely to die use the neurotransmitter acetylcholine in their synapses.
Research suggests that insulin resistance facilitates the aggregation of a protein called amyloid-beta in the hippocampus. These aggregations, or collections, of protein build up over time, forming amyloid-beta plaques. These plaques stimulate an immune response from microglia in the brain, which begins a cascade of cellular activity that damages neurons and prevents them from functioning normally. The neurons in the hippocampus eventually begin to die and, because the hippocampus is essential for forming memories, memory problems and dementia are common symptoms. Plaques also build up in the cerebral cortex and so neuronal death occurs there too. The neurons that are most likely to die use the neurotransmitter acetylcholine in their synapses.
Identifying and Treating Alzheimer’s disease
Increasing age is the major risk factor for the development of Alzheimer’s disease, although other risk factors exist. For example, having type 2 diabetes is thought to increase the risk of developing Alzheimer’s disease. Genetic risk factors exist too. Mutations in genes called PSEN1 and PSEN2 are associated with early-onset familial Alzheimer’s disease. Another genetic risk factor involves the type of apolipoprotein that you have. Apolipoproteins are normally required for transporting fats in the circulatory system, but having a type called E4 may lead to the formation of more amyloid-beta plaques.
There is currently no cure for Alzheimer's Disease, but some medications can ease the symptom of memory loss. An example of this type of medication is the AChE inhibitor. This medication works by preventing an enzyme from breaking down the neurotransmitter acetylcholine, which is found in some hippocampal and cortical synapses; because acetylcholine is not broken down, it stays in the synapse for longer, helping the neurons to continue to communicate and thus improving the symptom of memory loss.
If a person is diagnosed with Alzheimer's Disease, a comprehensive care plan will be drawn up. This involves more than just prescribing medication. Areas in which the patient needs or will need support are identified and addressed. This support comes in a number of ways and can include occupational therapy, psychological therapy (such as cognitive stimulation and relaxation therapy), patient and carer support and counselling.
There is currently no cure for Alzheimer's Disease, but some medications can ease the symptom of memory loss. An example of this type of medication is the AChE inhibitor. This medication works by preventing an enzyme from breaking down the neurotransmitter acetylcholine, which is found in some hippocampal and cortical synapses; because acetylcholine is not broken down, it stays in the synapse for longer, helping the neurons to continue to communicate and thus improving the symptom of memory loss.
If a person is diagnosed with Alzheimer's Disease, a comprehensive care plan will be drawn up. This involves more than just prescribing medication. Areas in which the patient needs or will need support are identified and addressed. This support comes in a number of ways and can include occupational therapy, psychological therapy (such as cognitive stimulation and relaxation therapy), patient and carer support and counselling.
Clinical Top Tip:
Cautions of AChEi
Galantamine and rivastigmine are two other types of acetylcholinesterase inhibitors. But the prescriber must be aware of these drugs, and donepezil, in patients who have bradycardia (heart rate less than 60bpm) or heart block, as they can further reduce the patient's heart rate.
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