Skip to content Skip to navigation

Elizabeth Mormino | Effects of aging and early Alzheimer’s pathology on cortical mechanisms of memory

Elizabeth Mormino, Stanford University
October 13, 2022 - 2:15pm to 3:00pm
Li Ka Shing Center / Paul Berg Hall or via livestream

Speaker

Elizabeth Mormino

Stanford University

Dr. Beth Mormino is a neuroscientist that applies multimodality imaging and biofluid techniques to understand disease progression and the neural correlates of behavioral and cognitive changes that occur in disease. Her primary research focus is on the intersection between Alzheimer’s disease (AD) and human aging.

Dr. Mormino completed a PhD in Neuroscience at UC Berkeley in the laboratory of Dr. William Jagust, where she performed some of the initial studies applying Amyloid PET with the tracer PIB to clinically unimpaired older individuals. During her postdoctoral fellowship with Drs. Reisa Sperling and Keith Johnson at MGH she investigated longitudinal cognitive trajectories in unimpaired individuals with abnormal Alzheimer’s biomarkers. In 2017, Dr. Mormino joined the faculty at Stanford University in the Department of Neurology and Neurological Sciences. She currently leads the Imaging Core of the Stanford Alzheimer’s Disease Research Center and the longitudinal extension of the Stanford Aging and Memory Study.

Session Overview

Effects of aging and early Alzheimer’s pathology on cortical mechanisms of memory

Multiple pathological processes interact with brain regions that support episodic memory, resulting in subtle performance differences well before overt clinical impairment. One common pathological pathway is Alzheimer’s disease, and it is established that both hallmark features of this disease are detectable in many older clinically unimpaired (CU) adults (amyloid plaques and tau tangles). Dr. Mormino's lab has demonstrated heterogeneity in spatial patterns of tau PET signal among CU in key cortical nodes relevant to visual associative memory processes (ventral temporal lobe, precuneus, inferior parietal). Along these lines, they find that cortical reinstatement during retrieval of associative pairs is reduced in CU with genetic risk of Alzheimer’s (APOE4+), and also shows trend level associations with global measures of abnormal tau in the cerebrospinal fluid. Interestingly, both abnormal tau and cortical reinstatement strength independently predict individual differences in overall memory performance, emphasizing the presence of multiple age-related pathways that influence cortical mechanisms of memory. .

Event Sponsor: 
Wu Tsai Neurosciences Institute
Contact Email: 
neuroscience@stanford.edu