INS NYC 2024 Program

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 early-life adversity 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 adulthood. Despite this, recent literature investigating the impacts of these adversities has focused primarily on White 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 57 participants 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 (CERAD) Word List Delayed Recall (WLDR). Early-life Adversity was measured using The Stress and Anxiety Inventory (STRAIN), 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 MMSE score 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 MMSE 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. However, cognitive performance was associated with hippocampal volume, a marker of neurodegeneration, a few years before dementia onset, typically 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 sample size are warranted to further examine the relationship among early-life adversity, neurodegeneration, and cognitive decline in those at increased risk for AD.