Almost 47 million people live with dementia worldwide, and that number is expected to reach 131 million in 2050, according to Alzheimer’s Disease International (ADI). Dementia due to Alzheimer’s disease (AD) is estimated to account for 60 to 80 percent of cases. Dementia affects about half of the population age 85 years or older.
AD begins with progressively worsening dysfunction in memory, cognition and behavior, and culminates in loss of all higher brain function and, eventually, death due to immobility. There is no cure, and treatment of symptoms provides only limited, temporary relief. Hence, the full force of academic brain researchers and the pharmaceutical industry have focused on achieving measurable changes in the brain function of patients afflicted by AD. A status report of those efforts will be highlighted beginning July 16 as the leading annual meeting—The Alzheimer’s Association International Conference—takes place in London.
The researchers at the meeting will spend a lot of time discussing one of the main strategies for intervention involving mitigation of the accumulation of aggregates formed mainly from amyloid beta (Aβ)—a peptide, or short chain of amino acids. Aβ appears in the cerebrospinal fluid, and its deposition in brain can be monitored via an imaging technique called amyloid positron emission tomography (aka “amyloid imaging” or “amyloid brain scanning”). Much of the pharmacological research is devoted to testing the hypothesis that reducing brain Aβ accumulation will prevent or slow the progression of memory problems. So far, the exclusive manipulation of Aβ levels in research and clinical trials has only resulted in a series of high-profile failures of drugs targeting Aβ.
In principle, the case for removing Aβ is strong. An Aβ mutation in certain Icelanders causes levels of that peptide to be reduced by half in the brain, blood and other tissues throughout their lives. These Icelanders virtually never…