In Search of Early Biomarkers of LATE, a Form of Dementia Related to TDP-43 Aggregation

LATE is a comparatively recently discovered form of dementia, connected to aggregation of misfolded TDP-43, one of the few proteins in the body capable of taking on an altered form that encourages other molecules of the same protein to also adopt that form and join together to form clumps. Aggregates are disruptive of cell function, but it is a slow process to understand exactly why this is the case. Researchers have been working on understanding amyloid-β aggregates for decades now, and continue to find that the present state of knowledge is incomplete regarding how the toxic halo of biochemistry that surrounds aggregates causes dysfunction and cell death. With the growing interest in TDP-43 pathology, researchers have in recent years found it present in many older people to a measurable degree, as is the case for other protein aggregates. It is important to work towards therapies that can clear all of these aggregates, such as potentially those based on the use of catabodies. Even in the absence of very obvious pathology, it is likely the case that protein aggregates contribute to brain aging in more subtle, indirect ways. Medin aggregates, for example, have only recently been found to likely cause pathology, and they have been known for decades. Looking for an Early Sign of LATE Limbic predominate age-related TDP-43 encephalopathy or LATE is a recently recognized form of dementia that affects memory, thinking, and social skills. It mimics Alzheimer'...
Source: Fight Aging! - Category: Research Authors: Tags: Medicine, Biotech, Research Source Type: blogs