2013Alzheimer s & DementiaRequires access

P2–206: Cerebral amyloid angiopathy and its co‐occurrence with Alzheimer's disease in the National Alzheimer's Coordinating Center Neuropathology data set

Willa D. Brenowitz, Peter T. Nelson, Lilah M. Besser, Katherine Bristow, Walter A. Kukull

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Abstract

Cerebral amyloid angiopathy (CAA) is a common neuropathological finding among older adults, especially among those with Alzheimer's disease (AD), and is characterized by β-amyloid deposits in cerebral blood vessel walls. The prevalence of CAA in prior autopsy series of older adults has varied from 10–40% of normal brains to over 80% in brains with neuropathological AD. We aim to better characterize the prevalence of CAA and its correlates with AD neuropathology (ADNP). This sample consisted of 5,754 autopsied subjects from the National Alzheimer's Coordinating Center's Neuropathology Data Set who died from 2002–2012 and were aged 65+ years at death. Standardized clinical and neuropathology data were obtained from approximately 30 Alzheimer's Disease Centers (ADCs) in the U.S. Presence of CAA was detected using amyloid stains and overall severity of CAA was documented as none, mild, moderate or severe. Prevalence of CAA was estimated overall and stratified by Braak neurofibrillary tangle stage and CERAD neuritic plaque score as well as for each ADC, and age at death. Across all ADCs, CAA was diagnosed in 79% of subjects with high levels of ADNP (Braak stages V/VI and frequent neuritic plaques), and in 13.6% with no ADNP (no neurofibrillary degeneration and no neuritic plaques), although estimates varied between ADCs. Examining CAA severity by ADNP, we found that prevalence of moderate/severe CAA was higher than no CAA (44% vs. 23%) among subjects with frequent neuritic plaques; whereas, the prevalence of moderate/severe CAA was much lower than no CAA (3.7% vs. 82%) among subjects without neuritic plaques. Examining ADNP severity by CAA, we found that the prevalence of frequent neuritic plaques was much higher than no neuritic plaques (75% vs. 2.3%) among subjects with moderate/severe CAA, but was similar (30% vs. 39%) among subjects without CAA. Prevalence of CAA increased by age at death until age 85 and decreased thereafter in this sample of 5,754 autopsied individuals. We describe the percentage of NACC cases with CAA, ADNP, both, or neither. In sum, CAA and ADNP do not always co-occur. NACC data enables an evaluation of expected variation using a very large, multi-center sample of autopsied individuals.

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What this paper is about

Cerebral amyloid angiopathy (CAA) is a common neuropathological finding among older adults, especially among those with Alzheimer's disease (AD), and is characterized by β-amyloid deposits in cerebral blood vessel walls. The prevalence of CAA in prior autopsy series of older adults has varied from 10–40% of normal brains to over 80% in brains with neuropathological AD. We aim to better characterize the prevalence of CAA and its correlates with AD neuropathology (ADNP). This sample consisted of 5,754 autopsied subjects from the National Alzheimer's Coordinating Center's Neuropathology Data Set who died from 2002–2012 and were aged 65+ years at death. Standardized clinical and neuropathology data were obtained from approximately 30 Alzheimer's Disease Centers (ADCs) in the U.S. Presence of CAA was detected using amyloid stains and overall severity of CAA was documented as none, mild, moderate or severe. Prevalence of CAA was estimated overall and stratified by Braak neurofibrillary tangle stage and CERAD neuritic plaque score as well as for each ADC, and age at death. Across all ADCs, CAA was diagnosed in 79% of subjects with high levels of ADNP (Braak stages V/VI and frequent neuritic plaques), and in 13.6% with no ADNP (no neurofibrillary degeneration and no neuritic plaques), although estimates varied between ADCs. Examining CAA severity by ADNP, we found that prevalence of moderate/severe CAA was higher than no CAA (44% vs. 23%) among subjects with frequent neuritic plaques; whereas, the prevalence of moderate/severe CAA was much lower than no CAA (3.7% vs. 82%) among subjects without neuritic plaques. Examining ADNP severity by CAA, we found that the prevalence of frequent neuritic plaques was much higher than no neuritic plaques (75% vs. 2.3%) among subjects with moderate/severe CAA, but was similar (30% vs. 39%) among subjects without CAA. Prevalence of CAA increased by age at death until age 85 and decreased thereafter in this sample of 5,754 autopsied individuals. We describe the percentage of NACC cases with CAA, ADNP, both, or neither. In sum, CAA and ADNP do not always co-occur. NACC data enables an evaluation of expected variation using a very large, multi-center sample of autopsied individuals.

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Available abstract

Cerebral amyloid angiopathy (CAA) is a common neuropathological finding among older adults, especially among those with Alzheimer's disease (AD), and is characterized by β-amyloid deposits in cerebral blood vessel walls. The prevalence of CAA in prior autopsy series of older adults has varied from 10–40% of normal brains to over 80% in brains with neuropathological AD. We aim to better characterize the prevalence of CAA and its correlates with AD neuropathology (ADNP). This sample consisted of 5,754 autopsied subjects from the National Alzheimer's Coordinating Center's Neuropathology Data Set who died from 2002–2012 and were aged 65+ years at death. Standardized clinical and neuropathology data were obtained from approximately 30 Alzheimer's Disease Centers (ADCs) in the U.S. Presence of CAA was detected using amyloid stains and overall severity of CAA was documented as none, mild, moderate or severe. Prevalence of CAA was estimated overall and stratified by Braak neurofibrillary tangle stage and CERAD neuritic plaque score as well as for each ADC, and age at death. Across all ADCs, CAA was diagnosed in 79% of subjects with high levels of ADNP (Braak stages V/VI and frequent neuritic plaques), and in 13.6% with no ADNP (no neurofibrillary degeneration and no neuritic plaques), although estimates varied between ADCs. Examining CAA severity by ADNP, we found that prevalence of moderate/severe CAA was higher than no CAA (44% vs. 23%) among subjects with frequent neuritic plaques; whereas, the prevalence of moderate/severe CAA was much lower than no CAA (3.7% vs. 82%) among subjects without neuritic plaques. Examining ADNP severity by CAA, we found that the prevalence of frequent neuritic plaques was much higher than no neuritic plaques (75% vs. 2.3%) among subjects with moderate/severe CAA, but was similar (30% vs. 39%) among subjects without CAA. Prevalence of CAA increased by age at death until age 85 and decreased thereafter in this sample of 5,754 autopsied individuals. We describe the percentage of NACC cases with CAA, ADNP, both, or neither. In sum, CAA and ADNP do not always co-occur. NACC data enables an evaluation of expected variation using a very large, multi-center sample of autopsied individuals.

Key concepts: Neuropathology, Senile plaques, Cerebral amyloid angiopathy, Neurofibrillary tangle, Alzheimer's disease, Pathology, Autopsy, Medicine

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P2–206: Cerebral amyloid angiopathy and its co‐occurrence with Alzheimer's disease in the National Alzheimer's Coordinating Center Neuropathology data set — Research Paper | ScholarLens