Alzheimer as a disease
Alzheimer’s disease is categorised by the loss of function in brain cells. This could lead to the eradication of brain cells entirely. Brain functions that are affected include memory loss, change in thought process, as well as gradual and slow loss of mobility. This damage in brain cells accounts for 60 to 80 per cent of cases of dementia.
Symptoms and diagnosis
The symptoms are different for everyone, although there are commonalities experienced in most situations. A common indicator is the inability to retain new information. The regions of the brain dedicated to building new memories are usually the places where initial damage occurs.
As time progresses, the spread of the disease causes other loss of function. Typical symptoms include loss of memory that interferes with day-to-day activities, difficulty with planning and making resolutions, challenges in recognising special relationships and visual images, avoidance of social activities, anxiety, and insomnia. There is a decline in cognitive functions with time. Individuals would need assistance in conducting daily activities. Severe cases lead to bed-bound care. This inactivity and reduced mobility increase the chance of infections that are detrimental to the immune system.
There is no straight-forward method to diagnose Alzheimer. With the assistance of a neurologist, various tests are carried out. A medical history and background of the patient are required—this is a predictor for the chance of having Alzheimer. Family and friends are confronted with identifying any changes in thinking pattern and skills. Blood tests and brain scans are also used to verify traces of dementia. Lastly, neurological, cognitive and physical examinations are conducted.
Brain's transformation with Alzheimer
Alzheimer manifests in the form of tangles (also known as tau tangles) or plaques (beta-amyloid plaques). Tangles “interfere with vital processes." Plaques are deposits over a scattered area that can be toxic in the brain at high levels. In both scenarios, it hinders the transfer of information between neurons in the form of synapses. The flow of signals in the brain are also responsible for thought processes, emotions, mobility, and skills. The absence of synapses results in the death of neurons. Beta-amyloid obstruct the flow of synapses. While the tau tangles deter nutrients and important molecules within the neuron. The brain scan of individuals affected by Alzheimer usually show images of debris from the death of neurons and cells, inflammation, and shrinkage of regions of the brain due to cell loss.
Pharmaceutical Treatment – Aducanumab and AADva-1
Alzheimer's treatments often target the beta-amyloid. It is the main component of developing plaques. There are two enzymes that are responsible for secreting beta-amyloid; beta-secretase and gamma-secretase. Memory loss associated with Alzheimer occurs with the accumulation of beta-amyloid and tau triangles. Nevertheless, it takes between 15 to 20 years before there is a notable effect on memory. It is crucial to interfere with processes involved in forming beta-amyloid plaques. This includes blocking the enzyme’s activity in creating plaques, reducing the formation of beta-amyloid aggregates, and the use of antibodies to break down beta-amyloid across the brain. Previous studies showed that most drugs in phase 3 trial, failed to have a correlation between reduced amount of beta-amyloid proteins and delay in cognitive decline.
The biotechnology organization, Biogen Idec were successful in passing phase one for the drug, aducanumab. The study underwent in phase one is geared to test the tolerance and safety of the drug. Phase one trials occur over a small group of people and within the period of six months to a year. The health status of individuals involved in the phase one trial includes individuals with beta-amyloid present in the brain and others that experienced early stages of Alzheimer.
Aducanumab is a monoclonal antibody against the buildup of beta-amyloid. The antibody acts as a tag and signals the immune system to destroy beta-amyloid cells. Prior to treatment, a PET scan helps in quantifying the presence of beta-amyloid proteins. It is hypothesised that reducing levels of beta-amyloid will improve cognition in the individual. Based on the results, it was concluded that aducanumab is a dose-dependant drug. An increased dose had a greater effect in reducing beta-amyloid plaques.
One of the flaws of this drug trial is that not every patient showed signs of beta-amyloid formation in the brain. Not everyone experienced the benefit of the medication. Additionally, not all patients experienced cognitive decline. Individuals had most of their functions intact. A loss of function in cognition is associated with the death of neurons. Therapies that involves antibodies aim at destroying the growth of plaques rather than regenerating lost neurons.
Promising feedback of the phase one trial debunks other therapies. Although medications have aided in reducing the number of plaques, Aducanumab is the first antibody therapy that targets slowing down cognitive decline.
It is important to point out that the sample size of the phase one trial is relatively small. Therefore, the phase three clinical trial is significant for the larger crowd of patients. Phase three clinical trials will test the effectiveness of the drug in large populations. Another concern is the approximate cost of the medication. It is expected for the Alzheimer patient to spend about $40,000 a year for treatment.
AADva-1 incorporates an active vaccine to trigger the immune response to tau proteins. The result is degradation of the protein. The phase one trial was composed of 30 patients showing mild to moderate levels of Alzheimer disease. A single dose of injections was administered every month. Here the safety, tolerance and immune response of the medication was examined. As of March 2016, the phase two trial began. It involved about 185 patients. The injections were administered to test cognitive functions, safety, and immune response in the individual. The phase three clinical trial is in the process. This stage is tailored to ensure that ADDva-1 can stop the formation of tau protein aggregates.
Non-pharmacological treatment involves engaging the patient in daily activities to keep the mind and body active. It also encourages social participation and retained memory function. Examples include art therapy, memory training programs, and activity-based therapy. However, there is less research evidence on the impact of non-pharmacological treatment as opposed to medication in Alzheimer patients.
Most people affected with Alzheimer experience dependability and disability with the illness. This is reinforced by the unpaid hours and out-of-pocket cost of family member caregivers. There is a tremendous demand for a reliable treatment of Alzheimer. It is a key to improve the quality of lives of individuals and support their daily activities.