Promising early results of new drugs that target common components of several brain diseases that cause dementia – including Alzheimer's disease, Parkinson's disease, and Lewy Body dementia – were reported at the Alzheimer's Association International Conference® 2015 (AAIC® 2015).

These diseases cause a range of debilitating symptoms, including memory loss, difficulty with language, visual hallucinations or problems with movement, but they all share the same hallmark – the death of brain cells. Many diseases that cause brain cell death and dementia share common characteristics. One is that a particular protein goes through a dramatic change in its shape; often it becomes toxic for nerve cells or the brain connections known as synapses.

Today, 47 million people are living with dementia worldwide, and that number is set to almost double by 2030 and more than triple by 2050, according to Alzheimer's Disease International.

When proteins misfold, they can start off a chain reaction of binding to other proteins. This process continues until large aggregates are formed. Two different misfolded proteins – amyloid beta and tau – have been shown to be toxic to brain cells. Their large aggregates – amyloid plaques and tau tangles – are the hallmark brain lesions of Alzheimer's disease. Treatments that target more than one Alzheimer's-related protein may be especially useful in managing the disease.

"Alzheimer's is very complex condition that has been extremely hard to address with the 'one target, one treatment' approach that's been successful in other diseases," said Maria Carrillo, PhD, Alzheimer's association Chief Science Officer. "Fortunately, we're beginning to see some very exciting early results at AAIC 2015 of a new treatment approach that targets common components of all the Alzheimer's proteins, which also are common to other diseases that cause dementia. If these results can be shown in people, this strategy could eventually have benefit not just in Alzheimer's but for other neurodegenerative diseases."

It is generally agreed that the cause of several neurodegenerative diseases is related to the accumulation of proteins in aggregated (or oligomeric, where several proteins are bound together) forms. Disease-causing forms of these proteins can also change normal proteins into destructive forms, allowing toxic malformations to spread to different areas of the brain.

Fernando Goni, PhD, Adjunct Associate Professor, Department of Neurology, New York University School of Medicine, New York NY and colleagues announced new data at AAIC 2015 about a class of monoclonal antibodies that were shown to react to both amyloid and tau in Alzheimer's disease, and also to prion disease proteins. They report that the antibodies may also react to aggregated alpha-synuclein and other structures (known as Lewy Bodies) in the brain cells of people with Parkinson's disease, suggesting a potentially broad range of beneficial effects in neurological diseases.

To establish the effect of their antibodies on various forms of alpha-synuclein, the researchers created single alpha-synuclein proteins, oligomeric alpha-synuclein proteins, and dense fibrillar forms known to accumulate in brain tissue. The researchers then tested their antibodies to see how they interacted with each form of alpha-synuclein. Three types of monoclonal antibodies from their laboratory were used, each of which binds to amyloid and tau and also reverses Alzheimer's-like damage to brain tissue in animals. They found that all three monoclonal antibodies bind to the oligomeric forms of alpha-synuclein but not to the monomeric forms. They subsequently confirmed the antibodies' affinity for alpha-synuclein related structures within neurons using samples of human brain tissue from individuals with Parkinson's disease.

"We have developed monoclonal antibodies that recognize the toxic oligomeric proteins from multiple diseases that cause brain cell death and dementia," said Goni. "This is very promising. We are now at a point where we can test them in other animal models as a precursor to clinical trials for human neurodegenerative diseases."