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 #60 Associations Between Physical Activity and Markers of Alzheimer’s Disease Pathology in Non-Demented Carriers of Autosomal Dominant Alzheimer’s Disease Angelys Rivera-Hernández, University of Puerto Rico-Río Piedras, San Juan, Puerto Rico Edmarie Guzmán-Vélez, Massachusetts General Hospital, Harvard Medical School, Boston, United States Clara Vila-Castelar, Massachusetts General Hospital, Harvard Medical School, Boston, United States Stephanie Langella, Massachusetts General Hospital, Harvard Medical School, Boston, United States Diana Munera, Massachusetts General Hospital, Harvard Medical School, Boston, United States Ana Baena, Grupo de Neurociencias de Antioquia, Facultad de Medicina, Universidad de Antioquia, Medellín, Colombia Jairo Martinez, Massachusetts General Hospital, Harvard Medical School, Boston, United States Averi Giudicessi, Massachusetts General Hospital, Harvard Medical School, Boston, United States Francisco Lopera, Grupo de Neurociencias de Antioquia, Facultad de Medicina, Universidad de Antioquia, Medellín, Colombia Yakeel Quiroz, Massachusetts General Hospital, Harvard Medical School, Boston, United States Category: Dementia (Alzheimer's Disease) Keyword 1: dementia - Alzheimer's disease Keyword 2: genetic neuropsychology Keyword 3: quality of life Objective: Alzheimer’s disease (AD) is a neurodegenerative disease without a cure that leads to dementia. AD-related pathology (e.g., amyloid, tau) starts accumulating decades before the onset of memory impairment, i.e., preclinical stage. Physical activity has been suggested as a promising lifestyle factor that could protect against memory impairment, as it has been associated with slower neurodegeneration and cognitive decline in older adults. Yet, there is limited data on its relationship to disease progression and memory in people in the preclinical stage of AD. We addressed this gap by examining the association between physical activity and blood-based markers of AD in a Colombian kindred with autosomal-dominant AD (ADAD) due to a mutation (E280A) in Presenilin-1 (PSEN1) who typically develop mild cognitive impairment at a median age of 44 years and dementia at 49 years. We hypothesized that greater physical activity would be related to better memory and lower levels of AD pathology markers. Participants and Methods: 19 PSEN1 E280A mutation carriers (C; ages: μ=31.16 years, SD: 4.94) and 42 non-carriers (NC; ages: μ=35.57 years, SD: 5.99) wore a FitBit watch for 14 consecutive days. 37 participants were female. We calculated their Training Impulse (TRIMP), a measure of the total time spent engaging in physical activity, using their daily heart rate and minutes spent engaging in at least moderate activity. Lower TRIMP means less physical activity. Participants also completed the Consortium to Establish a Registry for AD word list learning and delayed recall. Markers of AD pathology (phosphorylated Tau-181; ptau-181), neural injury (neurofilament light chain; NfL), and neuroinflammation (C-Reactive protein; CRP, YKL-40, and interleukin; IL-6) were measured in plasma. Linear regressions were used to examine associations of TRIMP levels with CERAD word list test scores and plasma markers. Statistical significance was assessed using independent sample t-tests. Results: Mutation carriers exhibited less TRIMP levels compared to non-carriers (p=0.04). TRIMP levels were not associated with sex or age. There was a trend-level association between TRIMP levels and NfL in the carriers (C: r=0.08, p=0.06; NC: r=0.5253, p=0.71). Also, mutation carriers with higher TRIMP levels showed increased p-tau181 levels (p=0.03). TRIMP levels were not related memory performance, nor with plasma markers of CRP, YKL-40, or IL-6 (ps>0.05). Conclusions: These preliminary findings suggest that physical activity intensity may not have a significant impact on memory or plasma markers of neural injury and inflammation in preclinical ADAD. However, associations may be observed in later stages of the disease, as most mutation carriers were in the very early stages of AD. Physical activity showed a trend-level association with NfL levels that may be due to the small sample size. More research is needed to understand the association of increased p-tau181 levels with high physical activity in this population. Longitudinal data in larger samples will be critical for further characterizing the role of physical activity in AD progression.

Poster

02/16/2024
01:45 pm - 03:00 pm
Room: Shubert Complex (Posters 1-60)

Poster Session 08: Cognition | Cognitive Reserve Variables

Final Abstract #60

Associations Between Physical Activity and Markers of Alzheimer’s Disease Pathology in Non-Demented Carriers of Autosomal Dominant Alzheimer’s Disease

Angelys Rivera-Hernández, University of Puerto Rico-Río Piedras, San Juan, Puerto Rico
Edmarie Guzmán-Vélez, Massachusetts General Hospital, Harvard Medical School, Boston, United States
Clara Vila-Castelar, Massachusetts General Hospital, Harvard Medical School, Boston, United States
Stephanie Langella, Massachusetts General Hospital, Harvard Medical School, Boston, United States
Diana Munera, Massachusetts General Hospital, Harvard Medical School, Boston, United States
Ana Baena, Grupo de Neurociencias de Antioquia, Facultad de Medicina, Universidad de Antioquia, Medellín, Colombia
Jairo Martinez, Massachusetts General Hospital, Harvard Medical School, Boston, United States
Averi Giudicessi, Massachusetts General Hospital, Harvard Medical School, Boston, United States
Francisco Lopera, Grupo de Neurociencias de Antioquia, Facultad de Medicina, Universidad de Antioquia, Medellín, Colombia
Yakeel Quiroz, Massachusetts General Hospital, Harvard Medical School, Boston, United States

Category: Dementia (Alzheimer's Disease)

Keyword 1: dementia - Alzheimer's disease
Keyword 2: genetic neuropsychology
Keyword 3: quality of life

Objective:

Alzheimer’s disease (AD) is a neurodegenerative disease without a cure that leads to dementia. AD-related pathology (e.g., amyloid, tau) starts accumulating decades before the onset of memory impairment, i.e., preclinical stage. Physical activity has been suggested as a promising lifestyle factor that could protect against memory impairment, as it has been associated with slower neurodegeneration and cognitive decline in older adults. Yet, there is limited data on its relationship to disease progression and memory in people in the preclinical stage of AD. We addressed this gap by examining the association between physical activity and blood-based markers of AD in a Colombian kindred with autosomal-dominant AD (ADAD) due to a mutation (E280A) in Presenilin-1 (PSEN1) who typically develop mild cognitive impairment at a median age of 44 years and dementia at 49 years. We hypothesized that greater physical activity would be related to better memory and lower levels of AD pathology markers.

Participants and Methods:

19 PSEN1 E280A mutation carriers (C; ages: μ=31.16 years, SD: 4.94) and 42 non-carriers (NC; ages: μ=35.57 years, SD: 5.99) wore a FitBit watch for 14 consecutive days. 37 participants were female. We calculated their Training Impulse (TRIMP), a measure of the total time spent engaging in physical activity, using their daily heart rate and minutes spent engaging in at least moderate activity. Lower TRIMP means less physical activity. Participants also completed the Consortium to Establish a Registry for AD word list learning and delayed recall. Markers of AD pathology (phosphorylated Tau-181; ptau-181), neural injury (neurofilament light chain; NfL), and neuroinflammation (C-Reactive protein; CRP, YKL-40, and interleukin; IL-6) were measured in plasma. Linear regressions were used to examine associations of TRIMP levels with CERAD word list test scores and plasma markers. Statistical significance was assessed using independent sample t-tests.

Results:

Mutation carriers exhibited less TRIMP levels compared to non-carriers (p=0.04). TRIMP levels were not associated with sex or age. There was a trend-level association between TRIMP levels and NfL in the carriers (C: r=0.08, p=0.06; NC: r=0.5253, p=0.71). Also, mutation carriers with higher TRIMP levels showed increased p-tau181 levels (p=0.03). TRIMP levels were not related memory performance, nor with plasma markers of CRP, YKL-40, or IL-6 (ps>0.05).

Conclusions:

These preliminary findings suggest that physical activity intensity may not have a significant impact on memory or plasma markers of neural injury and inflammation in preclinical ADAD. However, associations may be observed in later stages of the disease, as most mutation carriers were in the very early stages of AD. Physical activity showed a trend-level association with NfL levels that may be due to the small sample size. More research is needed to understand the association of increased p-tau181 levels with high physical activity in this population. Longitudinal data in larger samples will be critical for further characterizing the role of physical activity in AD progression.