Hopes up! Is successful Alzheimer’s disease treatment now possible?

Alzheimers header

Lately, we have talked a lot about Alzheimer’s disease and how devastating a dementia diagnosis can be – not only for the person with the disease, but also for their loved ones. For people who have never experienced dementia, forgetfulness can be interpreted as an endearing sign of seniority, but when a loved one has more and more trouble remembering familiar people, surroundings, or even the passage of time – the seriousness of the situation becomes clear.

Hopes up!
Now it’s time for some good news: A recent study, published in The Journal of Experimental Medicine gets our hopes up for a complete reversal of Alzheimer’s disease one day.

Alzheimer’s disease is characterized by the deposition of amyloid plaques in the brain, neurofibrillary tangles, progressive loss of synapses and severe cognitive dysfunction (1, 2). Accumulation of beta-amyloid peptides is one of the initial steps that lead to the development of Alzheimer’s disease pathologies. Now, researchers have found that deleting a specific enzyme called beta-secretase (BACE1) in mice led to the reversal of pre-formed amyloid plaque deposition and actually improves the animals’ cognitive function (3).

Why BACE1?
BACE1 is a beta-secretase that cleaves amyloid precursor protein (APP) producing beta-amyloid, the main component of the amyloid plaques found in the brain which disrupt the function of neuronal synapses (Figure 1).

Figure 1: Figure represents normal and Alzheimer's brain sections, displaying formation of Amyloid plaques during Alzheimer’s disease.

Figure 1: Figure represents normal and Alzheimer’s brain sections, displaying formation of Amyloid plaques during Alzheimer’s disease.


Drugs that inhibit BACE1 are being developed as potential Alzheimer’s disease treatments but as BACE1 controls many important processes by cleaving proteins other than APP, these drugs could have serious side effects. To investigate the effects, researchers have generated conditional knockout mice that lose BACE1 function in adulthood, to mimic BACE1 inhibitor treatment in Alzheimer’s patients. These conditional knockout mice developed normally without neurodevelopmental defects and that they remained healthy. The BACE1 mutant mice were then bred with mice that were showing amyloid plaques and Alzheimer’s disease at an approximate age of 2 months. The next generation mice, initially formed amyloid plaques which began to disappear with age and complete loss of BACE1 activity (3).

This study not only shows that with a loss of BACE1, pre-formed amyloid deposition can be reversed completely in adult mice but also that decreasing BACE1 activity reversed other hallmarks of Alzheimer’s disease, such as the activation of microglial cells and the appearance of abnormal neuronal processes. The complete loss of BACE1, indeed improved cognitive functions, such as learning and memory, but only partially restored synaptic function, suggesting that BACE1 may be still be an important factor for optimal synaptic activity (3). Even though further studies will be required, this study gives us hope that BACE1 inhibition could be very beneficial for Alzheimer’s disease patients and shows that we are at an exciting stage of Alzheimer’s drug development.

Visit QIAGEN’s Alzheimer’s Disease Pathway to get full insights of the network of genes involved in the amyloid metabolism. Explore our Neurodegenerative Disease Research Center for further information and a comprehensive overview of sample and assay technologies enabling exponential advances in Alzheimer’s Disease research.


1. Braak, H., and E. Braak. Diagnostic criteria for neuropathologic assessment of Alzheimer’s disease Neurobiol Aging. 1997 Jul-Aug; 18(4 Suppl):S85-8. (link)
2. Corriveau, R.A., et al. 2017. Alzheimer’s Disease-Related Dementias Summit 2016: National research priorities. American Academy of Neurology (link)
3. Xiangyou Hu; et al. 2018 BACE1 deletion in the adult mouse reverses preformed amyloid deposition and improves cognitive functions. Journal of Experimental Medicine jem.20171831; DOI: 10.1084 (link)

Laura Alina Mohr, M.Sc.

Laura Alina Mohr joined QIAGEN in 2015. She received her Master’s Degree in Chemical Biology at the Technical University Dortmund in Germany. During this time, she was involved in Systemic Cell Biology research at the prestigious Max Planck Institute. Before joining QIAGEN, Laura Alina worked at the Scripps Research Institute, San Diego, where she first focused on DNA damage/repair pathways and telomere biology. Later, she joined the Muscle Development, Aging and Regeneration program at the Sanford Burnham Prebys Medical Discovery Institute. At QIAGEN she is interested in gene expression profiling focusing on various biological pathways, e.g. cancer research and neurodegeneration.

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