Alzheimer’s and Society
Alzheimer’s disease is often invisible. It is not uncommon for families and friends to unconsciously ignore the warning signs, or to choose to hide the disease of a loved one. Due to a pervasive lack of awareness and no proper understanding of the condition, stigmatisation prevails. With over 60% of healthcare practitioners worldwide considering dementia a part of normal aging, families are the main care providers for Alzheimer’s patients, which strains them physically, emotionally and financially.
Over 55 million people worldwide live with dementia, the main cause of dependency among the old population. Alzheimer’s disease accounts for over 60% of cases. The 2025 World Alzheimer’s Report draws attention to the importance of rehabilitation programmes, which can improve the patients’ quality of life, by delaying loss of independence.
About half of the US$ 1.3 trillion healthcare cost of dementia (or over 80 billion caregiving hours yearly) is represented by informal care, i.e. families and friends. In low income settings, this proportion climbs to 80%. This is further aggravated by an accelerated rise in the number of patients in middle and low income countries.
Up to ¾ of people suffering from dementia do not receive a diagnosis, hence no treatment or specialised care. This situation is difficult to address, because 75% of WHO member states do not have a national dementia plan, which means a lack of medical infrastructure, no up-to-date medical workforce training and no community support.
Why Tau? Why Now?
At molecular level, we can imagine Alzheimer’s disease looking like a tangle of microscopic octopus tentacles (the tau tangles) that caught minuscule bushes of seaweed here and there (the amyloid plaques). The result: neurons loose their synaptic plasticity, cells suffer from neuroinflammation and mitochondrial dysfunction.
In healthy brains, tau proteins stabilize the transport of celullar components along the axon of a neuron, thus maintaining its function and survival. Disruptions in this axonal transport are associated with various neurological disorders, including Alzheimer's disease. In affected brains, tau proteins leave their microtubules (which make possible the axonal transport), and create the tau tangles. But tau tangles are extremely stable, thus difficult to break. Targeting tau before it gets tangled – let’s call them “tau seeds” – reduces the toxic build-up associated with Alzheimer’s disease.
There is growing consensus that amyloid alone is insufficient as a therapeutic target: 20+ amyloid targeting trials failed to prove cognitive benefits. The correlation between tau tangles buildup and cognitive decline is stronger than in case of amyloid plaques. Tau therapies (currently in clinical trials) offer multiple intervention points (aggregation inhibitors, immunotherapy, degradation systems like LYTACs, dephosphorylation via PP2A) and are adequate for multimodal strategies. Advances in protein engineering (like LYTACs) and optogenetics allow fine-tuned intracellular modulation (e.g. TauTuner).
Introducing Promnesis, an innovative
therapeutic system that
combats Alzheimer’s from its core.
Logic Gates: Diagnosis and Targeted Therapeutic Release
TRI-LYTAC: A TRIple LYsosome TArgeting Chimera
TauTuner: Inducible, Reversible Tau Dephosphorylation
In its mature form, Promnesis would be a therapeutic system for Alzheimer’s disease. The constructs (logic-gated promoters controlling LYTACs and optogenetic phosphatases) would be packaged into PEGylated lipid vesicles, which can cross the blood–brain barrier and deliver the therapy into neurones and glial cells. Once inside the brain, the system would detect stress signals and selectively clear toxic phosphorylated tau, thus restoring cells' functions.
Explore our project
Project Description
Software
Engineering
Results
Human Practices