Neuropathology of Alzheimer's Disease
Open accessAbstract
Alois Alzheimer first pointed out that the disease which would later bear his name has a distinct and recognizable neuropathological substrate. Since then, much has been added to our understanding of the pathological lesions associated with the condition. The 2 primary cardinal lesions associated with Alzheimer's disease are the neurofibrillary tangle and the senile plaque. The neurofibrillary tangle consists of abnormal accumulations of abnormally phosphorylated tau within the perikaryal cytoplasm of certain neurons. The senile plaque consists of a central core of beta‐amyloid, a 4‐kD peptide, surrounded by abnormally configured neuronal processes or neurites. Other neuropathological lesions are encountered in cases of Alzheimer's disease, but the disease is defined and recognized by these 2 cardinal lesions. Other lesions include poorly understood changes such as granulovacuolar degeneration and eosinophilic rodlike bodies (Hirano bodies). The loss of synaptic components is a change that clearly has a significant impact on cognitive function and represents another important morphological alteration. It is important to recognize that distinguishing between Alzheimer's disease, especially in its early stages, and normal aging may be very difficult, particularly if one is examining the brains of patients who died at an advanced old age. It is also noted that instances of pure forms of Alzheimer's disease, in the absence of other coexistent brain disease processes, such as infarctions or Parkinson's disease–related lesions, are relatively uncommon, and this must be taken into account by researchers who employ postmortem brain tissues for research. Mt Sinai J Med 77:32&–42, 2010. © 2010 Mount Sinai School of Medicine
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Eosinophilic Hirano bodies, granulovacuolar degeneration, and cerebral amyloid angiopathy are common in Alzheimer's disease.
“Additionally eosinophilic Hirano bodies, granulovacuolar degeneration (GVD) and cerebral amyloid angiopathy (CAA) are also common [18, 23].”
From The neuropathological diagnosis of Alzheimer's disease (2019) · cites this paper as [18]
The sections on granulovacuolar degeneration and vascular amyloid deposition associate both lesions with Alzheimer's disease. The Hirano bodies section says they occur in smaller numbers in “some, but not all” Alzheimer's cases, so the source does not clearly support calling all three lesions common. The supplied passages have section labels but no page numbers. (LLM, conf=0.84)
Experimental — accuracy not yet measuredSevere cerebral amyloid angiopathy can impair blood flow and produce ischemic lesions or small infarcts, and can lead to lobar hemorrhages typically affecting the frontal and occipital lobes.
“Severe CAA can impair blood flow and produce ischemic lesions or small infarcts, while severe CAA can lead to lobar hemorrhages typically affecting the frontal and occipital lobes [18].”
From The neuropathological diagnosis of Alzheimer's disease (2019) · cites this paper as [18]
The “Vascular Amyloid Deposition” section supports the hemorrhage portion: severe vascular involvement can cause rupture, with hemorrhages tending to occur at the frontal or occipital poles; large ones are called lobar hemorrhages. It says amyloid deposits do not appear to obstruct vessels or interfere with their function, so it does not support impaired blood flow or CAA-caused infarcts. The “Alzheimer’s Disease and Its Associated Conditions” section describes ischemic infarcts as a coexisting condition, not a consequence of CAA. Page numbers were not supplied. (LLM, conf=0.88)
Experimental — accuracy not yet measuredVascular dementia represents the most common concurrent pathology in AD.
“It represents the most common concurrent pathology in AD [18, 113, 114].”
From The neuropathological diagnosis of Alzheimer's disease (2019) · cites this paper as [18]
In “Alzheimer’s Disease and Its Associated Conditions” (page unavailable), the paper identifies stroke, specifically ischemic infarction, as the most common coexisting condition with AD. It calls cases with both AD and infarction “mixed dementia” but does not establish vascular dementia itself as the most common concurrent pathology. (LLM, conf=0.84)
Experimental — accuracy not yet measuredAmyloid deposits in cerebral amyloid angiopathy are enriched in Aβ40 while parenchymal deposits are enriched in Aβ42 species.
“Amyloid deposits in CAA are enriched in Aβ40 (while parenchymal deposits are enriched in Aβ42 species) and can affect small arteries, arterioles and even capillaries of the gray matter of the cerebral cortices and in leptomeningeal vessels [18, 23].”
From The neuropathological diagnosis of Alzheimer's disease (2019) · cites this paper as [18]
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“Introduction Alzheimer’s disease (AD) is a neurodegenerative disease characterized by chronic progressive dementia, and its hallmark pathological changes include amyloid beta (Aβ) plaques, intracellular neurofibrillary tangles, and neuronal loss.(1) The clinical diagnostic criteria of AD mainly rely on symptoms, scale…”
Background
- Authors
- Perl, D. P.
- Affiliations
- Icahn School of Medicine at Mount Sinai (US)
- Corresponding author
- Perl, Daniel P.
- ORCID
- Perl, Daniel P.
- Venue
- Mount Sinai Journal of Medicine: A Journal of Translational and Personalized Medicine
- Publisher
- Wiley
- Published
- 2010-01
- Volume
- 77
- Issue
- 1
- Pages
- 32-42
- ISSN
- 0027-2507 (ISSN-L)
- 1931-7581
- PMC
- PMC2918894
- OpenAlex
- W2070448139
- Cited by
- 825
- References
- 62
- Citations by year
- 2026: 34 · 2025: 65 · 2024: 61 · 2023: 80 · 2022: 65 · 2021: 80 · 2020: 95 · 2019: 50 · 2018: 51 · 2017: 34 · 2016: 45 · 2015: 33 · 2014: 35 · 2013: 27 · 2012: 18
- FWCI
- 2.91
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Mount Sinai Journal of Medicine A Journal of Translational and Personalized Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging (P50AG005138, P01AG002219)
- 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, neuropathology, neurofibrillary tangles, amyloid plaques, tau phosphorylation, amyloid-beta, granulovacuolar degeneration, Hirano bodies, synaptic loss, postmortem brain
- MeSH terms
- Alzheimer Disease, Brain, Brain Diseases, Humans, Amyloid beta-Peptides, Neurofibrillary Tangles, 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.
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