Poster | Poster Session 08 Program Schedule
02/16/2024
01:45 pm - 03:00 pm
Room: Shubert Complex (Posters 1-60)
Poster Session 08: Cognition | Cognitive Reserve Variables
Final Abstract #38
Associations Among Early-Life Adversity, Hippocampal Volume, and Cognitive Performance in Non-Demented Individuals With Autosomal Dominant Alzheimer’s Disease
Elizabeth Kaplan, Massachusetts General Hospital, Harvard Medical School, Boston, United States Stephanie Langella, Massachusetts General Hospital, Harvard Medical School, Boston, United States Ana Baena, Grupo de Neurociencias de Antioquia, Universidad de Antioquia, Medellin, Colombia Diana Munera, Massachusetts General Hospital, Harvard Medical School, Boston, United States Jairo Martinez, Massachusetts General Hospital, Harvard Medical School, Boston, United States Averi Giudicessi, Massachusetts General Hospital, Harvard Medical School, Boston, United States Alex Badillo Cabrera, Massachusetts General Hospital, Harvard Medical School, Boston, United States Nikole Bonillas Felix, Massachusetts General Hospital, Harvard Medical School, Boston, United States George Slavich, Massachusetts General Hospital, Harvard Medical School, Los Angeles, United States Sergio Alvarez, Hospital Pablo Tobon Uribe, Medellin, Colombia Fransisco Lopera, Grupo de Neurociencias de Antioquia, Universidad de Antioquia, Medellin, Colombia Yakeel Quiroz, Massachusetts General Hospital, Harvard Medical School, Boston, United States
Category: Dementia (Alzheimer's Disease)
Keyword 1: cognitive functioning
Objective:
Elevated incidences of early-life adversity have been linked to reduced hippocampal volume and heightened deficits in cognitive functioning in older individuals; however, the associations between and risk for Alzheimer’s Disease (AD), specifically, remain unclear. Latino children are disproportionately exposed to early-life adversities compared with white children and thus, may be at a greater risk of subsequent hippocampal degeneration and cognitive impairment in older Despite this, recent literature investigating the impacts of these adversities has focused primarily on participants. In the present investigation, we examined early-life adversity and its relationship with hippocampal volume and cognitive performance in individuals from Colombia who belong to families with autosomal dominant AD (ADAD).
Participants and Methods:
A total of from the Massachusetts General Hospital (MGH) Colombia-Boston (COLBOS) Biomarker Study were included (mean age = 39.9 years, SD = 6.38). Cognitive performance was measured using the Mini-Mental State Examination (MMSE) and the Consortium to Establish a Registry for Alzheimer's Disease () Word List Delayed Recall (WLDR). , specifically the Time Limited: Total count of Early Adversity (EATotCT) measure (range:0-10). Structural MRI scans were conducted at MGH. MRI images were processed with FreeSurfer (v6.0). Pearson correlations and regression models, adjusted for sex, age, and intracranial volume, were used to elucidate associations among early-life adversity, hippocampal volume, and cognitive performance.
Results:
Participants had a mean of 28.6 (SD=1.29) and mean EATotCT score of 3.79 (SD=2.75). There were no significant associations among early-life adversity, hippocampal volume, and cognitive performance (all Ps>0.05). However, hippocampal volume was positively correlated with both total MMSE (r=0.43, p=0.002) and WLDR scores (r=0.35, p=0.014). Results from regression models were consistent with correlation analyses, showing that higher hippocampal volume was associated with higher and WLDR scores.
Conclusions:
Our findings suggest that early-life adversity did not exhibit significant associations with either hippocampal volume or cognitive performance in adults who belong to families with ADAD. cognitive performance was associated with hippocampal volume, a marker of neurodegeneration, a few years before , at age 49 for members of these ADAD families. Limitations in the STRAIN such as cultural bias, subjective and retrospective reporting, and response bias may have influenced these results. Furthermore, this inventory does not account for protective factors that individuals may have had in their lives, which could mitigate the impact of adversity. Future investigations which address these limitations through the implementation of multiple measures of early-life adversity and which utilize a larger size are warranted to further examine the relationship among early-life adversity, neurodegeneration, and cognitive decline in those at increased risk for AD.
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