TDP43

ALS │ FTD │ LATE │CTE

Several neurodegenerative diseases are characterized by the accumulation of misfolded deposits of a protein called TDP43. This protein is thought to contribute to disease pathogenesis and its deposits are a hallmark sign of the devastating disease called Amyotrophic Lateral Sclerosis (ALS) as well as Frontotemporal Dementia (FTD), a neurodegenerative disease that is genetically and mechanistically related to ALS.  TDP43 pathology is also present to varying degrees in other neurodegenerative conditions, most notably a disease related to Alzheimer’s Disease (AD) called Limbic-predominant Age-related TDP43 Encephalopathy (LATE), and Chronic Traumatic Encephalopathy (CTE), a neurodegenerative condition resulting from repeated head trauma.  Because of its central role in the pathogenesis of these diseases, TDP43 is viewed as a high value target for biomarker development. Unfortunately, there are currently no approved technologies to detect TDP43 in CNS or peripheral tissues.

Alpha synuclein

PD │ LBD │ MSA

Misfolding and subsequent deposition of the presynaptic protein a-synuclein into aggregates is a defining feature of a spectrum of diseases called the synucleinopathies.  These include Parkinson’s Disease (PD), a neurodegenerative disease of the motor system and a major cause of dementia affecting ~1% of people over 60 years of age, and other devastating diseases such as Lewy Body Dementia (LBD) and Multiple System Atrophy (MSA). Much like TDP43 in ALS, a-synuclein is viewed as a high value molecular biomarker that could greatly facilitate diagnosis and monitoring of the disease if it can be detected and measured. However, like TDP43, technologies for detecting this key biomarker in CNS are lacking.

Amyloid Beta

AD │ CAA │ TBI │ CAA│ GLC

The accumulation of amyloid beta is a hallmark feature of Alzheimer’s Disease (AD) and a related disease called Cerebral Amyloid Angiopathy (CAA), a condition that sometimes co-exists with AD.  Amyloid beta deposits also form in brain after a traumatic brain injury (TBI), which is a known risk factor for AD.  While amyloid beta deposition in brain can be detected and quantified using PET scanning, this procedure has inherent limitations related to cost, radiation exposure and the need to utilize specialized imaging centers that curtail its broad and repeated utilization. Amyloid beta deposits can also be present in some retinal diseases, such as Age-related Macular Degeneration (AMD) and glaucoma. While current ocular imaging cameras are able to detect structural and vascular changes in the retina associated with these eye diseases, molecular biomarker detection is lacking (PET imaging of amyloid beta is not applicable to the eye). The Amydis tracer technology augments the capabilities of existing modalities by enabling the detection of molecular changes that likely precede structural and vascular changes.