Alzheimer’s disease is a progressive neurological deterioration that occurs in middle to old age (MacGill, 2016). It is the most common form of dementia, a disorder which prevails when the brain is damaged by certain diseases. It has been estimated Alzheimer’s disease contributes to 60–70% of dementia cases (WHO, 2012). The figures reflecting the incidence of dementia are truly striking. In 2015, there were around 46.8 million cases globally. By 2050, this is set to increase to 131.5 million (Alzheimer’s Disease International, 2015). An epidemic is an unusually high number of cases of a disease. The above figures appear to fit this criterion.
For Alzheimer’s to be considered a global epidemic it is important to investigate the incidence across the world. Figure 1 shows this clearly. The World Alzheimer Report (2015) suggests that much of the increase will occur in low and middle income countries (LMICs). By 2050, 68% of dementia sufferers will be in LMICs. This is a cause for concern as these regions may be without quality healthcare thus symptoms could go unnoticed, meaning that the true incidence may be underestimated. Also, life expectancy is increasing worldwide. This is associated with the increase in incidence of Alzheimer’s. The World Alzheimer Report (2015) also estimated that between 2015 and 2050 the number of older people in high income countries will increase by 56%. This figure seems to be large but it is low compared to the estimated 239% increase in low income countries. This is worrying due to the possibility of lower availability of health and social care, meaning these countries may find it more difficult to cope with an epidemic.
As a neurodegenerative disease, Alzheimer’s is characterised by progressive neuronal death (MacGill, 2016). There are several changes in the brain but these are unfortunately only found post mortem. One such change is the amyloid plaques found between dying neurones. There is some understanding of how these plaques form and this understanding could be applied to treatment. The plaques contain a large amount of β- amyloid (Aβ), a membrane protein synthesised at the endoplasmic reticulum (ER). Aβ is produced from the amyloid precursor protein which is synthesised at the ER and delivered to the plasma membrane. One pathway in which this precursor protein is cleaved is harmful and leads to Alzheimer’s disease. Mutations in the genes encoding the amyloid precursor protein and one of the cleavage enzymes, Y-secretase, are factors that increase the amount of harmful Aβ peptides and thus increase the risk of developing Alzheimer’s. Aβ forms amyloid plaques because of its tendency to aggregate. It is not certain whether these plaques are causal or just a symptom of Alzheimer’s. However, studies in mice have suggested that these plaques cause Alzheimer’s disease. Most studies agree that pathological criteria such as amyloid plaques account for 40% to 70% of the variance in cognition (O’Brien and Wong, 2011).
Alzheimer’s affects the patient, their family and carers, and the economy. While Alzheimer’s affects every patient differently, the cognitive effects can be generalised to illustrate how difficult this disease can be for sufferers. The earliest symptoms are related to memory loss (Alzheimer’s Society, 2017). This is due to damage to the hippocampus, the region of the brain associated with memory. This memory loss can be distressful and can also lead to difficulties in carrying out daily activities. Even in the early stages, a change in the mood of the patient is observed. As the disease progresses, symptoms tend to worsen. Patients tend to live for eight to ten years after they first express symptoms. As there is currently no cure, this creates a huge burden for the patient.
Patients require a wide range of care. The difficulty with this is that it spans a wide range of healthcare and social care, meaning that the quality of care of a patient is a shared responsibility between different sectors. As a result, several different individuals may be responsible for the care and treatment of one patient. Unless communication is sufficient, this could put a strain on both sectors. The mental deterioration associated with Alzheimer’s results in largely full time care. It has been estimated that 43% cases require care equivalent to a nursing home (Brookmeyer et al., 2017). This causes multiple socioeconomic problems to surface. More health and social care professionals are required, along with more facilities. Families may provide care at home. This is classified as informal care and is vital in many cases, reducing the strain on healthcare and social care professionals (Winblad et al., 2016). However, the pressure of informal care may reduce the quality of life for the family and the time commitment may not be feasible. If Alzheimer’s is to become a global epidemic, the consequences for families may be some of the most severe. For care to be as effective as possible, diagnosis needs to be rapid.
Alzheimer’s has a significant impact on the economy. In 2014, the direct cost of Alzheimer’s in USA was estimated to be $214 billion, and this is the impact on only one country. To truly investigate the economic effects, it is important to look at the breakdown of expenditure. In 2010, globally only 16% of costs were medical costs, 41.7% were informal care costs and 42.3% were formal care costs. This is disheartening as it shows that the need to care for patients because of their lost cognitive function is currently more crucial than finding a cure.
Dementia can almost always be diagnosed (Alzheimer’s Association, 2017). Simple tests include the mini mental state examination (MMSE). Following indicative results from this, brain scans may be used. Computerised tomography (CT) and magnetic resonance imaging (MRI) scans show structural changes to brain tissue. It can be difficult to determine what the exact cause of dementia is, making it difficult to specifically diagnose Alzheimer’s disease. Diagnosis of Alzheimer’s is a lengthier process. The patient’s medical history must be available. Their mental state must be assessed, along with a physical and neurological exam. Brain scans may then be used to rule out other causes of dementia-like symptoms. It is estimated that a skilled physician can diagnose Alzheimer’s with over 90% accuracy. More recently, the possibility of specific diagnosis through biomarkers has been researched (Reiman et al., 2012). A biomarker is a measurable indicator of a condition in the body. Aβ accumulation can be used as a biomarker as the proteins can be measured using brain imaging. However, the above procedures may not be achievable in a country with poor healthcare. The consequences of this must be considered. For example, an individual without a detailed medical history may not receive early diagnosis. Thus, they are less likely to benefit from treatment, if available, and support for themselves and their family.
The global pressure resulting from Alzheimer’s could be lessened if there was a cure. Although there is currently no cure, research has been conducted into medication to treat cognitive symptoms. Cholinesterase inhibitors prevent the degradation of acetylcholine, the parasympathetic nervous system neurotransmitter (Larkin, 1998). Higher levels of acetylcholine enhance communication between neurones and, importantly, improve learning and memory. For example, one drug called metrifonate improves behavioural symptoms and cognition. These treatments are prescribed in earlier stages of Alzheimer’s thus recognition of symptoms early on is crucial. A potential cause for Alzheimer’s becoming an epidemic is the lack of drugs available. There have been multiple cases where patients are given new hope by research into a drug, only for it to fail before getting to market. Solanezumab was a trial drug that was developed to target early stages of Alzheimer’s, but this trial was halted (Karran and Hardy, 2014). This drug is a monoclonal IgG1 antibody targeting soluble Aβ peptides that are toxic to neurons. In November 2016, after completing the first 3 phases, the trial was terminated based on a lack of positive results. This is not an isolated event, several other drugs targeting various stages of Alzheimer’s haven’t reached completion.
Recently another suggested treatment has arisen, targeting the Aβ peptides using metal complexes which can cleave them (Derrick et al., 2017). These complexes would target the harmful Aβ42 isoforms of the peptide. A promising metal complex is composed of a cobalt (II) metal center bound to a tetra-N-methylated cyclam ligand. This complex is named Co(II)(TMC). It has been shown to cleave peptides and prevent them from aggregating. In addition, this complex has potential blood- brain barrier permeability meaning it could act directly on Aβ peptides in the brain. If this technique is successful and reaches human trial it could be a breakthrough regarding the prevention of a global epidemic. By controlling the aggregation of Aβ peptides, the progression of Alzheimer’s could be slowed.
The increasing prevalence of Alzheimer’s disease cannot be ignored. The fact that it is increasing globally supports the ideology that it is becoming, if it has not already become, a global epidemic. With an ageing population and no confident cure or preventative techniques the situation will worsen. Arguably, we are not yet experiencing a global epidemic. However, the projected figures for 2050 show that without advances in medicine it will surely become one. Of course, if a cure were to be found the impact would be dramatically reduced. In this scenario, the disease could not be considered a global epidemic.