According to a report by World Health Organization (WHO), the world’s population who are over 65 years old would estimate to increase by over 1.5 billion by 2050 and it would take 16.2% of the whole global population. The increase in the old population will induce various degenerative diseases including dementia. Alzheimer’s disease (AD) is the most common type of dementia, which accounts for 60 ~ 80% of all dementia cases. AD induces a decrease in memory, lingual capability, cognitive ability, and judgment, and patients with severe symptoms. If the symptom becomes worse, the patients are hard to keep their general life without others’ help and finally will die.

The brains of AD patients are shrunk compared to normal brains by extensive loss of neurons and there are pathoanatomically many senile plaques and neurofibrillary tangles in the brain. Neuronal cell death is induced by abnormal neurofibrillary tangle, which is known as the major reason why extensive neuronal loss is found in the AD brains. Neurofibrillary tangles are mainly composed of amyloid beta (Aβ) aggregates, which are often found in senile plaques. Aβ is generated from amyloid precursor protein through serial cleavage by beta and gamma secretases and composed with 39 to 42 amino acids. Aβ is not toxic to neurons as the status of monomer, but easily forms aggregates which are highly harmful to neurons. If the Aβ aggregates accumulate in the brain, they induce the loss of neuronal function as well as neuronal cell death.

Tau protein is known as a component of intracellular cytoskeleton, which plays an important role in stabilization cytoskeletal structure in neurons. Under pathological conditions, tau is separated from cytoskeletal structure and paired helical filaments by forming coagulates. Tau filament accumulation induces neuronal cell death and is directly related the symptoms of AD.

So far, 4 drugs have been prescribed to treat AD but all of them are symptom-reducing drugs, which have only very limited effects. Recently, aducanumab, a biologic based on an antibody specific for Aβ, was approved to treat AD but is controversial due to several issues, including low efficacy and toxicity. There are still huge unmet medical needs in the AD therapeutics market.

Before the appearance of symptoms of AD, Aβ aggregates and tau fibrils are already started accumulating. So, it is very important to remove Aβ/tau aggregates from the brain tissue to treat AD. So far, almost development of the therapeutic drug was focusing on prohibiting aggregate formation and did not succeed in improving cognitive decline. To treat AD efficiently, it is strategically required to dissociate or solubilized Aβ aggregates in the brain. SBC105 is a new conceptual drug for AD treatment, which can solubilize already exiting Aβ aggregates and tau fibrils as well as inhibit aggregate formation. SBC105 significantly improved reduced spatial cognitive ability in animal models induced by infusion of Aβ aggregates.