Biomarkers.

Background: Autosomal dominant Alzheimer disease (ADAD) is characterized by genetic mutations affecting the beta-amyloid (Aβ) pathway. However, vascular and immune factors play important roles which are not completely understood. Understanding the function of the neurovascular unit (NVU) comprised of neurons, glial cells, and vasculature, at different disease stages appears ideal to developing and evaluating therapeutics.

Biomarkers.

Background: Autosomal Dominant Alzheimer's Disease (ADAD) is a rare and early-onset form of Alzheimer's disease with a familial pattern of inheritance. While the pathological features of ADAD, such as amyloid plaques and neurofibrillary tangles, have been extensively studied, the involvement of white matter (WM) neuroinflammation is not well-explored. In sporadic AD, the hindered ratio (HR) derived from diffusion basis spectrum imaging (DBSI) has been used to study neuroinflammation in WM.

Biomarkers.

Background: The use of biomarkers for early detection of Alzheimer disease (AD) is crucial for developing potential treatments. As neurons die, brain structures, including the hippocampus, shrink and the cerebrospinal fluid spaces ventricles expand. However, due to its small size, hippocampal volumes can be challenging to measure.

Alzheimer's Imaging Consortium.

Background: Autosomal dominant Alzheimer disease (ADAD) is characterized by genetic mutations affecting the beta-amyloid (Aß) pathway. However, vascular and immune factors play important roles which are not completely understood. Understanding the function of the neurovascular unit (NVU) comprised of neurons, glial cells, and vasculature, at different disease stages appears ideal to developing and evaluating therapeutics.

Alzheimer's Imaging Consortium.

Background: Signal Peptide Peptidase-Like 2b (SPPL2b) is relevant for AD, being a brain-specific intramembrane protein involved in the cleavage of Alzheimer's disease (AD)-related proteins, such as BRI2, inflammatory-related proteins like CD74, TNFalpha, and Clec7a, and synaptic proteins Neuregulin-1 and VAMP 1-4. SPPL2b is specifically expressed in the hippocampus and cortex. The cleavage of TNFalpha by SPPL2b promotes the inflammatory pathway.