Neuropathology of preclinical and clinical lateonset Alzheimer's disease
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We report on the neuropathological examinations of a 74‐year‐old woman with Alzheimer's disease (AD) and of her 47‐year‐old nondementd daughter. The brain of the mother showed fully developed pathological changes of AD. By contrast, the brain of the daughter revealed only perineuronal deposition of diffuse amyloid in cerebral cortex and striking abnormalities of the endosomallysosomal system, without neurofibrillary, glial, or microglial changes. These observations suggest that amyloid deposition and endosomal‐lysosomal changes are early events in late‐onset AD and that they may precede the onset of dementia of several decades.
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The validity of the concept of a preclinical stage in Alzheimer's disease is supported by longitudinal clinical studies of mild memory changes followed by an accelerated decline and by clinical-pathological studies that report the presence of the characteristic lesions of Alzheimer's disease in cognitively normal individuals.
“The validity of the concept of a preclinical stage in AD is supported by longitudinal clinical studies of mild memory changes followed by an accelerated decline [6,15,19,33] and by clinical-pathological studies that report the presence of the characteristic lesions of AD in cognitively normal individuals [1,23,35,36].”
From Hippocampal neurons in pre-clinical Alzheimer's disease. (2004) · cites this paper as [36]
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Experimental — accuracy not yet measuredSome studies suggest that Aβ deposits in the brain may precede the onset of cognitive decline by a decade or more, indicating a wide temporal window for neuronal protective therapeutic intervention.
“Some of these studies suggest that the A deposits in the brain may precede the onset of cognitive decline by a decade or more [27,36], indicating the presence of a wide temporal window for neuronal protective therapeutic intervention.”
From Hippocampal neurons in pre-clinical Alzheimer's disease. (2004) · cites this paper as [36]
Senile plaques and neurofibrillary tangles in nondemented older adults may represent Alzheimer disease before clinical expression, with lesions accumulating over many years before synaptic and neuronal damage produces symptoms.
“Alternatively, the presence of SPs and NFTs in nondemented older adults may represent AD at a stage prior to its clinical expression,(Morris et al., 1996; Price & Morris, 1999; Troncoso et al., 1998; Hulette et al., 1998; Schmitt et al., 2000) in which the neuropathological lesions of AD accumulate over many years before sufficient synaptic and neuronal damage occurs to produce the symptoms of AD.”
From Neuropathology of nondemented aging: presumptive evidence for preclinical Alzheimer disease (2009) · cites this paper as Troncoso et al., 1998
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Self-citationAlzheimer's Disease in Males: Endocrine Issues and Prospects
Lerner, A. J. (1999) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.84.10.3416 · Cited by 7 · see citing works
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What Can We Learn About Alzheimer’s Disease from People with Down Syndrome?
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Combinatorial Methods to Engineer Small Molecules for Functional Genomics
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Exploring temporal and sex-linked dysregulation in Alzheimer disease phosphoproteome
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β-Amyloid Imaging In Vivo and Its Possible Implications for Alzheimer’s Disease
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Medication Use in Alzheimer's Disease and Healthy Aging
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Amyloid-beta alters trafficking of internalized acetylcholinesterase and dextran.
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Original Article Amyloid-beta alters trafficking of internalized acetylcholinesterase and dextran
Hu, W. T., Gray, N. W., Brimijoin, S., & Mn, R. (2009)
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- Authors
- Troncoso, J. C., Cataldo, A. M., Nixon, R. A., Barnett, J. L., Lee, M. K., Checler, F., Fowler, D. R., Smialek, J. E., Crain, B., Martin, L. J., & Kawas, C. H.
- Affiliations
- Johns Hopkins University (US)
- Harvard University (US)
- State of Maryland (US)
- Corresponding author
- Troncoso, Juan C.
- Venue
- Annals of Neurology
- Publisher
- Wiley
- Published
- 1998-05
- Volume
- 43
- Issue
- 5
- Pages
- 673-676
- ISSN
- 0364-5134 (ISSN-L)
- 1531-8249
- OpenAlex
- W2084221243
- Semantic Scholar
- 4e7b8290c80fc069a8bf626dbbe18b09a9dec369
- Cited by
- 93
- References
- 19
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 4 · 2023: 1 · 2022: 3 · 2020: 5 · 2019: 4 · 2018: 3 · 2016: 2 · 2015: 3 · 2014: 2 · 2013: 2 · 2012: 6
- FWCI
- 3.40
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Annals of Neurology (publishedVersion)
- PubMed (publishedVersion)
- eScholarship (California Digital Library) (submittedVersion, cc-by)
- Funders
- Johns Hopkins University
- National Institutes of Health (5r35ag010916-08)
- National Institute on Aging (AG 10916, P50AG005146, AG 05146)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, late-onset Alzheimer's disease, preclinical Alzheimer's disease, amyloid deposition, endosomal-lysosomal system, familial Alzheimer's disease, cerebral cortex, neurofibrillary tangles, dementia onset
- MeSH terms
- Aged, Alzheimer Disease, Amyloid, Family Health, Female, Frontal Lobe, Humans, Lysosomes, Middle Aged, Endosomes, Age of Onset, Pyramidal Cells, GTP-Binding Proteins, GTP Phosphohydrolases, rab5 GTP-Binding Proteins, Plaque, Amyloid
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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