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RETRACTED ARTICLE: A specific amyloid-β protein assembly in the brain impairs memory
27/27 checkable references clean · checked 2026-10-16
Every reference with a DOI in the deposited reference list resolved to a known work in Crossref or DataCite at the dated check, and none carried a retraction, withdrawal, or removal notice.
1 without a DOI — not checked. A reference deposited without a DOI is never matched by title or guessed at; it stays outside the checked set, and this line discloses that.
The 27 checked references that resolve
resolves10.1126/science.274.5284.99
Correlative Memory Deficits, Aβ Elevation, and Amyloid Plaques in Transgenic Mice
resolves10.1097/00005072-199709000-00002
APPSW Transgenic Mice Develop Age-related Aβ Deposits and Neuropil Abnormalities, but no Neuronal Loss in CA1
resolves10.1523/JNEUROSCI.21-02-00372.2001
Age-Dependent Changes in Brain, CSF, and Plasma Amyloid β Protein in the Tg2576 Transgenic Mouse Model of Alzheimer's Disease
resolves10.1523/JNEUROSCI.22-05-01858.2002
The Relationship between Aβ and Memory in the Tg2576 Mouse Model of Alzheimer's Disease
resolves10.1212/01.WNL.0000055813.36504.BF
Visual memory predicts Alzheimer’s disease more than a decade before diagnosis
resolves10.1073/pnas.090106797
Cerebral metabolic and cognitive decline in persons at genetic risk for Alzheimer's disease
resolves10.1056/NEJM200008173430701
Patterns of Brain Activation in People at Risk for Alzheimer's Disease
resolves10.1016/S0197-4580(99)00065-2
Evidence for glial-mediated inflammation in aged APPSW transgenic mice
resolves10.1038/35050110
Aβ peptide immunization reduces behavioural impairment and plaques in a model of Alzheimer's disease
resolves10.1038/35050103
A learning deficit related to age and β-amyloid plaques in a mouse model of Alzheimer's disease
resolves10.1073/pnas.96.6.3228
Plaque-independent disruption of neural circuits in Alzheimer’s disease mouse models
resolves10.1016/S0166-2236(00)01749-5
Targeting small Aβ oligomers: the solution to an Alzheimer's disease conundrum?
resolves10.1126/science.1079469
Common Structure of Soluble Amyloid Oligomers Implies Common Mechanism of Pathogenesis
resolves10.1523/JNEUROSCI.0462-04.2004
Cortical Synaptic Integration<i>In Vivo</i>Is Disrupted by Amyloid-β Plaques
resolves10.1016/j.neuron.2005.01.040
Intraneuronal Aβ Causes the Onset of Early Alzheimer’s Disease-Related Cognitive Deficits in Transgenic Mice
resolves10.1126/science.1113694
Tau Suppression in a Neurodegenerative Mouse Model Improves Memory Function
resolves10.1037/0735-7044.107.4.618
Severity of spatial learning impairment in aging: Development of a learning index for performance in the Morris water maze.
resolves10.1038/416535a
Naturally secreted oligomers of amyloid β protein potently inhibit hippocampal long-term potentiation in vivo
resolves10.1038/357500a0
Targeting of cell-surface β-amyloid precursor protein to lysosomes: alternative processing into amyloid-bearing fragments
resolves10.1007/BF03401708
Characterization of New Polyclonal Antibodies Specific for 40 and 42 Amino Acid-Long Amyloid β Peptides: Their Use to Examine the Cell Biology of Presenilins and the Immunohistochemistry of Sporadic Alzheimer’s Disease and Cerebral Amyloid Angiopathy Cases
resolves10.1046/j.1471-4159.2002.00901.x
Progressive decrease of amyloid precursor protein carboxy terminal fragments (APP‐CTFs), associated with tau pathology stages, in Alzheimer's disease
The 1 reference without a DOI — listed, not checked
no DOI — not checkedCraik, F. I. in Handbook of the Psychology of Aging (eds Birren, J. E. & Schall, K.) 384–420 (Van Nostrand-Reinhold, New York, 1977)
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