Alzheimer’s disease is the most common form of dementia, affecting approximately 35 million people worldwide. Alzheimer’s disease is a lethal disorder that also has a large impact on families and on the society. Today, preventive and disease modifying treatments are missing.
The underlying basis to why some people and not others develop the disease is not known, but an increasing body of scientific evidence suggests that the accumulation of amyloid plaques in the brain plays a pivotal pathogenic role in Alzheimer’s disease. The main risk factors to develop Alzheimer’s are age and genetic causes. Even though the disease can start as early as between 40 and 65 years of age, it is most common after 65 years.
Significant investments in Alzheimer research are being made because of the significant unmet medical need and the large cost of this disease for healthcare and society. The total global costs for dementia related diseases is estimated to about 1,000 billion USD globally in 2018. Given the lack of both effective symptomatic treatments and disease modifying treatments, the need for new effective therapies is acute.
The few approved drugs on the market today have only a limited symptomatic effect and can produce dose limiting side effects. A disease modifying treatment for Alzheimer’s disease is estimated to reach more than 10 billion USD in yearly sales. In Sweden, approximately 100 000 persons suffer from Alzheimer’s disease with a healthcare cost of about 63 billion SEK yearly, which is more than for cancer and cardiovascular diseases combined.
The video below gives a brief introduction to Alzheimer’s disease
Alzheimer’s disease results in neuronal dysfunction and death. The areas of the brain that usually are affected are the hippocampus, temporal and frontal lobes. During early stages of Alzheimer’s disease, so-called amyloid plaques build up and surround the neurons of the brain. The amyloid plaques hamper the normal function and viability of the neurons resulting in changed levels of neurotransmitters, which are critical chemical messengers needed for the communication between neurons. Acetylcholine is a very abundant neurotransmitter that is critical for cognitive function and which is reduced in Alzheimer’s disease. Other examples of neurotransmitters that are affected by Alzheimer are serotonin, noradrenaline and dopamine.
Alzheimer’s disease is a progressive neurodegenerative disorder. Typically, during early stages of the disease, areas involved in learning and memory are affected. Therefore, the most common early symptoms of Alzheimer’s disease are memory impairment and a particular difficulty in remembering newly learned information. As the disease advances through the brain, it leads to increasingly severe symptoms, including disorientation, mood and behavior changes; deepening confusion about events, time and place; unfounded suspicions about family and friends; more serious memory loss and behavior changes; and difficulty speaking, swallowing and walking.
Today there are two different classes of symptomatic drugs used for the treatment of Alzheimer’s disease:
- Acetylcholine esterase inhibitors: These drugs prolong the life of the neurotransmitter acetylcholine resulting in an improved communication between neurons.
- NMDA-inhibitor: This drug modifies the glutamate signaling pathway, which plays an essential role for the communication between neurons and for the learning process.
The effects seen by the treatments with Acetylcholine esterase inhibitors or NMDA inhibitors are often limited and associated with side effects, thus the need for novel therapies with better symptomatic effects and less side-effects are therefore urgent.
AlzeCure Pharma’s two programs NeuroRestore and Alzstatin have completely different mechanisms of action to treat the Alzheimer´s disease compared to the existing drugs. NeuroRestore improves the communications between neurons through a unique and very powerful mechanism involved in memory processing. Alzstatin, on the other hand, targets the actual disease and prevents the formation of toxic Aβ, the major constituent of amyloid plaques, thereby preventing or halting the neurodegenerative cascade.