MTHFR*677C>T produces distinct prodromal disease signatures in a mouse model of late-onset Alzheimer's disease
Background: Late-onset Alzheimer's disease (LOAD) comprises more than 95% of all AD cases. Transgenic, overexpression animal models have off target side effects, do not effectively produce the heterogeneity observed clinically in LOAD patients, and are therefore not best suited for preclinical therapeutic development. The Model Organism Development and Evaluation for Late-onset Alzheimer's…
A groundbreaking study in the field of Alzheimer's disease has unveiled new insights into a mouse model carrying the MTHFR*677C T variant. This variant, known to be associated with age-related cognitive decline, was combined with other humanized genetic factors in a novel transgenic mouse strain. Despite the absence of typical Alzheimer's hallmarks like amyloid plaques and neuroinflammation, the model exhibited distinctive brain patterns.
These patterns, which included altered gene expression and protein compositions, mirrored the cerebrovascular, myelination, and synaptic changes seen in human Alzheimer's patients. These findings underscore the potential of the LOAD2.Mthfr677C T mouse model as a valuable tool in preclinical therapeutic development for Alzheimer's disease, particularly in studying the impact of cerebrovascular compromise.
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