Evidence map›Paper›PMID 42630088›Full record

ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2026

Beyond amyloid: Contributions of neuroinflammation, cerebrovascular disease, and neurodegeneration to memory impairment in the oldest-old, the LifeAfter90 Study.

Batool Rizvi, Pauline Maillard, Alexander Ivan B Posis, Hilary L Colbeth, Nancy X Chen, Adam M Brickman, Paola Gilsanz, Maria M Corrada, Rachel A Whitmer

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Batool RizviDepartment of Public Health Sciences, University of California, Davis, Davis, California, USA.
Pauline MaillardDepartment of Neurology, University of California, Davis, Davis, California, USA.
Alexander Ivan B PosisDepartment of Public Health Sciences, University of California, Davis, Davis, California, USA.
Hilary L ColbethDepartment of Public Health Sciences, University of California, Davis, Davis, California, USA.
Nancy X ChenDepartment of Public Health Sciences, University of California, Davis, Davis, California, USA.
Adam M BrickmanTaub Institute for Research on Alzheimer's Disease and the Aging Brain, Vagelos College of Physicians and Surgeons, Columbia University, New York, New York, USA.
Paola GilsanzDivision of Research, Kaiser Permanente Northern California, Pleasanton, California, USA.
Maria M CorradaDepartment of Neurology, University of California, Irvine, Irvine, California, USA.
Rachel A WhitmerDepartment of Public Health Sciences, University of California, Davis, Davis, California, USA.

Funding

Epidemiology of Age-related Dementia, Mild Cognitive Impairment and Brain Pathology in Cohort of Oldest-OldR01AG056519 · NIA · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Maria Corrada, Paola Gilsanz · 2022 to 2026
$25.8M
UC Davis Alzheimer's Disease Research CenterP30AG072972 · NIA · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Charles DeCarli, Rachel A Whitmer · 2021 to 2026
$25.2M
National Institute on Aging of the National Institutes of Health P30AG072972National Institute on Aging of the National Institutes of Health R01AG056519NIA NIH HHS P30 AG072972NIA NIH HHS R01 AG056519Residual Class Settlement Funds Case 03-cv-2496
6 · The paper itself

Abstract

introductionNeuroinflammatory processes may play a central role in promoting mixed pathologies and cognitive impairment in the oldest-old. We hypothesize that elevated neuroinflammation, indicated by reactive astrocytosis, acts on cerebrovascular disease and separately, on amyloid beta (Aβ) pathology, to promote downstream medial temporal lobe atrophy and memory impairment.

methodsWe examined whether plasma glial fibrillary acidic protein (GFAP) concentration is associated with vascular territory-defined white matter hyperintensities (WMHs) on magnetic resonance imaging (MRI), global Aβ burden on positron emission tomography (PET), and episodic memory in a diverse cohort (N = 439) of the oldest-old: The LifeAfter90 Study.

resultsHigher plasma GFAP was associated with increased posterior cerebral artery (PCA)-defined WMH volume, but not with global amyloid or episodic memory. Both PCA WMH and global amyloid were associated with lower regional medial temporal lobe cortical thickness, which, in turn, was associated with episodic memory. DISCUSSION: These findings offer insights into new therapeutic and prevention strategies in the oldest-old population.

Indexed as

Amyloid beta-PeptidesCerebrovascular DisordersGlial Fibrillary Acidic ProteinMemory DisordersNeuroinflammatory DiseasesAged, 80 and overAtrophyFemaleHumansMagnetic Resonance ImagingMaleMemory, EpisodicPositron-Emission TomographyTemporal LobeWhite MatterAmyloid beta-PeptidesGFAP protein, humanGlial Fibrillary Acidic Proteinamyloidglial fibrillary acidic proteinmemoryneurodegenerationoldest‐oldwhite matter hyperintensities

Identifiers

PMID42630088
PMCPMC13498904

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.