Neuropathologic Studies of the Baltimore Longitudinal Study of Aging (BLSA)
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The Baltimore Longitudinal Study of Aging (BLSA) was established in 1958 and is one the oldest prospective studies of aging in the USA and the world. The BLSA is supported by the National Institute of Aging (NIA) and its mission is to learn what happens to people as they get old and how to sort out changes due to aging from those due to disease or other causes. In 1986, an autopsy program combined with comprehensive neurologic and cognitive evaluations was established in collaboration with the Johns Hopkins University Alzheimer's Disease Research Center (ADRC). Since then, 211 subjects have undergone autopsy. Here we review the key clinical neuropathological correlations from this autopsy series. The focus is on the morphological and biochemical changes that occur in normal aging, and the early neuropathological changes of neurodegenerative diseases, especially Alzheimer's disease (AD). We highlight the combined clinical, pathologic, morphometric, and biochemical evidence of asymptomatic AD, a state characterized by normal clinical evaluations in subjects with abundant AD pathology. We conclude that in some individuals, successful cognitive aging results from compensatory mechanisms that occur at the neuronal level (i.e., neuronal hypertrophy and synaptic plasticity) whereas a failure of compensation may culminate in disease.
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Aged individuals can harbor a high burden of AD brain lesions at autopsy while remaining cognitively intact, indicating resilience to AD pathology.
“several studies have revealed the existence of aged individuals harboring a high burden of brain lesions at autopsy while remaining cognitively intact, indicating resilience to AD pathology [3, 7, 21, 22, 56, 57, 68, 76, 78, 96].”
From Enhanced microglial dynamics and a paucity of tau seeding in the amyloid plaque microenvironment contribute to cognitive resilience in Alzheimer’s disease (2024) · cites this paper as [68]
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“However, several studies have revealed the existence of aged individuals harboring a high burden of brain lesions at autopsy while remaining cognitively intact, indicating resilience to AD pathology [3, 7, 21, 22, 56, 57, 68, 76, 78, 96].”
BackgroundSelf-citation
- Authors
- O'Brien, R. J., Resnick, S. M., Zonderman, A. B., Ferrucci, L., Crain, B. J., Pletnikova, O., Rudow, G., Iacono, D., Riudavets, M. A., Driscoll, I., Price, D. L., Martin, L. J., & Troncoso, J. C.
- Affiliations
- Department of Neurology, School of Medicine, Johns Hopkins University, Baltimore, MD, USA
- National Institutes of Health (US)
- Johns Hopkins University (US)
- Division of Neuropathology, Department of Pathology, Johns Hopkins University, Baltimore, MD, USA
- Fundación para la Lucha contra las Enfermedades Neurológicas de la Infancia (AR)
- ORCID
- Venue
- Journal of Alzheimer's Disease
- Publisher
- SAGE Publications
- Published
- 2009-10-30
- Volume
- 18
- Issue
- 3
- Pages
- 665-675
- ISSN
- 1387-2877 (ISSN-L)
- 1875-8908
- PMC
- PMC2978421
- OpenAlex
- W1498301041
- Cited by
- 137
- References
- 16
- Citations by year
- 2026: 1 · 2025: 9 · 2024: 12 · 2023: 10 · 2022: 4 · 2021: 16 · 2020: 12 · 2019: 7 · 2018: 9 · 2017: 9 · 2016: 6 · 2015: 9 · 2014: 9 · 2013: 7 · 2012: 8
- FWCI
- 3.49
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Alzheimer s Disease (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Johns Hopkins University
- National Institutes of Health
- National Institute on Aging (Z01AG000191, P50AG005146, AG 05146, ZIAAG000185)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Baltimore Longitudinal Study of Aging, autopsy
- MeSH terms
- Aged, Aged, 80 and over, Aging, Alzheimer Disease, Brain, Dementia, Female, Follow-Up Studies, Humans, Male, Parkinson Disease, Tissue Donors, Baltimore, Amyloid beta-Peptides, tau Proteins
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