Neuropathological alterations in Alzheimer disease
Open accessAbstract
The neuropathological hallmarks of Alzheimer disease (AD) include "positive" lesions such as amyloid plaques and cerebral amyloid angiopathy, neurofibrillary tangles, and glial responses, and "negative" lesions such as neuronal and synaptic loss. Despite their inherently cross-sectional nature, postmortem studies have enabled the staging of the progression of both amyloid and tangle pathologies, and, consequently, the development of diagnostic criteria that are now used worldwide. In addition, clinicopathological correlation studies have been crucial to generate hypotheses about the pathophysiology of the disease, by establishing that there is a continuum between "normal" aging and AD dementia, and that the amyloid plaque build-up occurs primarily before the onset of cognitive deficits, while neurofibrillary tangles, neuron loss, and particularly synaptic loss, parallel the progression of cognitive decline. Importantly, these cross-sectional neuropathological data have been largely validated by longitudinal in vivo studies using modern imaging biomarkers such as amyloid PET and volumetric MRI.
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Lewy pathology in AD is most frequent in olfactory bulb and amygdala.
“In particular, Lewy pathology in AD is most frequent in olfactory bulb and the amygdala [23, 123].”
From The neuropathological diagnosis of Alzheimer's disease (2019) · cites this paper as [23]
The “Overlap of AD with Lewy Body Disease” section reports Lewy-body-like inclusions in the amygdala and limbic structures in 70% of sporadic AD cases. It does not identify the olfactory bulb as a frequent site or compare sites to establish where Lewy pathology is most frequent. (LLM, conf=0.86)
Experimental — accuracy not yet measuredThe direct connection between Aβ and MAPT pathology is poorly understood, as shown by the weak correlation between the distribution of Aβ pathology and the distribution of MAPT pathology in humans.
“The direct connection between Aβ and MAPT pathology is poorly understood, as shown by the weak correlation between the distribution of Aβ pathology and the distribution of MAPT pathology in humans (Serrano-Pozo et al., 2011; Perez-Nievas et al., 2013; Scheltens et al., 2021).”
From β-amyloid accumulation enhances microtubule associated protein tau pathology in an APPNL-G-F/MAPTP301S mouse model of Alzheimer’s disease (2024) · cites this paper as Serrano-Pozo et al., 2011
The Topographic Distribution section says amyloid plaques accumulate mainly in the isocortex, unlike neurofibrillary tangles, and describes a particularly noticeable dissociation between their burdens in the medial temporal lobe. This supports the claim that their distributions differ in humans, but the cited passages do not establish that the direct connection between Aβ and tau pathology is poorly understood or report a correlation measure. (LLM, conf=0.82)
Experimental — accuracy not yet measuredSome dystrophic neurites associated with neuritic plaques contain tau filaments, which can have a paired helical filament morphology with electron microscopy.
“Some of the dystrophic neurites associated with neuritic plaques contain tau filaments, which can have a paired helical filament morphology with electron microscopy [23].”
From The neuropathological diagnosis of Alzheimer's disease (2019) · cites this paper as [23]
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 [23]
Dense cored neuritic plaques are accompanied by synaptic loss, activated microglia and reactive astrocytes.
“Dense cored NPs are also accompanied by synaptic loss, activated microglia and reactive astrocytes [23, 29, 36].”
From The neuropathological diagnosis of Alzheimer's disease (2019) · cites this paper as [23]
Amyloid 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 [23]
The parietal and occipital cortices are more vulnerable to cerebral amyloid angiopathy than the frontal and temporal lobes, and leptomeningeal arteries are more vulnerable than parenchymal vessels.
“Interestingly the parietal and occipital cortices are more vulnerable than the frontal and temporal lobes, and leptomeningeal arteries are more vulnerable than parenchymal vessels [23].”
From The neuropathological diagnosis of Alzheimer's disease (2019) · cites this paper as [23]
Alzheimer's pathology can be found in cognitively normal patients at autopsy, and this preclinical phase can also be observed in patients with mild cognitive impairment that do not meet criteria for clinical AD.
“Alzheimer’s pathology can be found in cognitively normal patients at the time of autopsy, and this preclinical phase can also be observed in patients with mild cognitive impairment that do not meet the criteria for clinical AD [4, 23].”
From The neuropathological diagnosis of Alzheimer's disease (2019) · cites this paper as [23]
Accumulation of amyloid-beta is a histological hallmark of the AD brain.
“Accumulation of amyloid-beta (Αβ) is a histological hallmark of the AD brain1.”
From Amyloid-β induces lipid droplet-mediated microglial dysfunction via the enzyme DGAT2 in Alzheimer’s disease (2025) · cites this paper as [1]
AD is the leading cause of dementia characterized by key neuronal hallmarks: extracellular deposition of Aβ plaques, formation of intracellular neurofibrillary tangles, and neuronal loss.
“AD is the leading cause of dementia characterized by key neuronal hallmarks: extracellular deposition of Aβ plaques, formation of intracellular neurofibrillary tangles, and neuronal loss (1, 2).”
From Modeling late-onset Alzheimer’s disease neuropathology via direct neuronal reprogramming (2024) · cites this paper as [1]
Neurodegeneration is a pathological hallmark of AD.
“Neurodegeneration is a pathological hallmark of AD 20 , which is exacerbated in a mouse model of tauopathy expressing APOE4 (refs. 12,21).”
From APOE4 impairs the microglial response in Alzheimer’s disease by inducing TGFβ-mediated checkpoints (2023) · cites this paper as [20]
The amyloid hypothesis of Alzheimer disease holds that excessive accumulation of amyloid-beta peptide leads to neurofibrillary tangles composed of aggregated hyperphosphorylated tau.
“The amyloid hypothesis of AD posits that excessive accumulation of amyloid-β peptide leads to neurofibrillary tangles composed of aggregated hyperphosphorylated tau84.”
From The use of brain organoids to investigate neural development and disease (2017) · cites this paper as [84]
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- Authors
- Serrano-Pozo, A., Frosch, M. P., Masliah, E., & Hyman, B. T.
- Affiliations
- Harvard University (US)
- University of California San Diego (US)
- Venue
- Cold Spring Harbor Perspectives in Medicine
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2011-09-01
- Volume
- 1
- Issue
- 1
- Pages
- a006189-a006189
- ISSN
- 2157-1422 (ISSN-L)
- PMC
- PMC3234452
- OpenAlex
- W2096963202
- Semantic Scholar
- 875ea5aa27548adac085b276cf2ba404af4ae139
- Cited by
- 3,345
- References
- 247
- Citations by year
- 2026: 150 · 2025: 269 · 2024: 316 · 2023: 343 · 2022: 348 · 2021: 379 · 2020: 318 · 2019: 261 · 2018: 263 · 2017: 214 · 2016: 168 · 2015: 137 · 2014: 101 · 2013: 44 · 2012: 26
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Cold Spring Harbor Perspectives in Medicine (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (AG5131, AG08487, NS057096, AG10435, AG18840)
- National Institute on Aging (AG18840, AG-08487, P01AG010435, R37AG018440, P50AG005131, AG-5131, R01AG008487, P50 AG05134, P01AG022074, AG22074, P50AG005134, U19AG010483, AG10435)
- National Institute of Neurological Disorders and Stroke (P30NS057096, NS057096)
- 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, amyloid plaques, cerebral amyloid angiopathy, neurofibrillary tangles, glial response, synaptic loss, neuronal loss, clinicopathological correlation, normal aging, cognitive decline, amyloid PET, volumetric MRI, imaging biomarkers
- MeSH terms
- Aging, Alzheimer Disease, Humans, Magnetic Resonance Imaging, Cerebral Amyloid Angiopathy, Neurofibrillary Tangles, Lewy Body Disease, Positron-Emission Tomography, Plaque, Amyloid, Cognitive Dysfunction
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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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