Beyond amyloid and tau: New targets in developing dementia treatments

Alzheimer’s disease is the most common form of dementia. Although its exact cause is unknown, for many years scientists have believed that a protein called beta-amyloid was responsible. Recently, this amyloid hypothesis has been questioned, and there has been a huge upsurge in dementia research. Here, we round up the latest findings, look at possible advances in diagnosis, and ask: Where next for Alzheimer’s research and treatment?

close-up of researcher's masked and goggled profile

Beta-amyloid and tau

Beta-amyloidTrusted Source is a peptideTrusted Source formed from a larger protein, called amyloid precursor proteinTrusted Source (APP). APP is a type 1 membrane glycoprotein that is involved in the development and function of nerve cells, signaling, and transport within cells.

When enzymes cut APP into smaller molecules, beta-amyloid monomersTrusted Source are one of the products. These monomers are likely to be important in maintaining the health of nerve cellsTrusted Source. The problems occur when beta-amyloid aggregates into fibrils and plaquesTrusted Source, which many researchers believe play a large part in the development of Alzheimer’s.

The amyloid cascade hypothesis, first proposed in 1992, suggested that amyloid plaques were the first stage in the development of Alzheimer’s, leading to neurofibrillary tanglesTrusted Source (tau tangles), cell loss, vascular damage, and dementia.

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