To make IMPRiND research accessible to a broader public, the IMPRiND glossary explains the main terms which are not necessarily known by all readers.
A general term referring to progressive diseases of the brain that are typically age-related and caused by loss of connections between neurons and ultimately their death. Neurons are the building blocks of the nervous system which includes the brain and spinal cord. Neurons normally don’t reproduce or replace themselves, so a disease process that cause the death of these cells leads to progressive loss of brain function such as the inability to form new memories in Alzheimer's disease (AD) or the slowness of movements in Parkinson's disease (PD).
These are protein clumps that are made of numerous molecules of the same protein that has lost its normal conformation and as a consequence became sticky and clustered to form a larger complex. Once formed, such assemblies can act as templates to induce the incorporation of further molecules inside cells or when taken up by neighbouring cells.
Tau is an abundant neuronal protein which under normal physiological conditions plays an important role in stabilizing microtubules which are involved in maintaining the structural integrity of the cell.
Alpha-synuclein is also an abundant neuronal protein and although it is functionally less understood it is thought to play an important role in the release of neurotransmitter. In neurodegenerative disease, tau and α-synuclein have abnormal conformations and can no longer carry out their normal function. The conversion of normal tau and α-synuclein into abnormal assemblies is believed to result in the development of AD and PD pathology, respectively.
Prion-like properties of tau and α-synuclein refer to mechanisms by which those assemblies spread throughout the brain in experimental models that resemble the way real prions become infectious agents. At the molecular level, this is linked to the ability of these proteins to form proteopathic assemblies and in this way initiate a chain reaction of amplification in a similar way as prion proteins. There is no evidence that AD and PD are due to infectious prions in humans.
The process whereby single molecules of a protein assemble together to forms larger structures.
Refers to potential therapeutic intervention points at which propagation of misfolded tau and α-synuclein can be prevented. These intervention points may be targeting mechanisms by which tau or α-synuclein assemblies are taken up by the the cell, destroyed by the cell or released.

This project receives funding from the Innovative Medicines Initiative 2 Joint Undertaking ( under grant agreement No 116060. This Joint Undertaking receives support from the European Union’s Horizon 2020 research and innovation programme and EFPIA.

This work is supported by the Swiss State Secretariat for Education‚ Research and Innovation (SERI) under contract number 17.00038.

The opinions expressed and arguments employed herein do not necessarily reflect the official views of these funding bodies.

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