Each study has a usefulness score out of 100 (rubric version 4.0). Tap a score to see what makes it up.
Download bibliography of all 5,209 studies, highest score first: BibTeX (.bib) · RIS (.ris)
Highest usefulness score first. Studies without a score come last.
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These results provide evidence that, in the absence of significant neurodegenerative processes, individuals who harbor AD neuropathology may remain cognitively unimpaired.
Why it matters
Among 79 older adults, those with Alzheimer's disease pathology but unimpaired cognition had lower levels of neurofilament light and total tau than those with Alzheimer's dementia, while levels of YKL-40 and neurogranin were not significantly different from controls. This suggests that neurodegeneration and synaptic dysfunction markers, rather than amyloid or tau alone, distinguish people with dementia from those with pathology but preserved cognition.
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Cerebrospinal fluid (CSF) biomarkers have been used to increase the evidence of underlying Alzheimer's disease (AD) pathology in mild cognitive impairment (MCI).
Why it matters
In 197 patients with mild cognitive impairment, adding the CSF Aβ42/40 ratio to the biomarker profile increased the predictive value for underlying Alzheimer's disease dementia. This is a diagnostic and prognostic study and does not test any treatment, cure, or prevention.
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AF is associated with greater cognitive decline and increased risk of dementia, independent of ischemic stroke.
Why it matters
Over 20 years, participants who developed atrial fibrillation had a greater decline in global cognitive score and a higher risk of dementia than those without it, after adjusting for cardiovascular risk factors including ischemic stroke. This identifies atrial fibrillation as a risk factor but does not test whether treating it prevents dementia.
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The precise mechanism through which many of these genes are associated with AD remains unknown.
Why it matters
This study looked at whether the top 20 known Alzheimer's risk genes are linked to amyloid buildup in the brain, using brain scans from 977 people. It found that these genes may affect Alzheimer's brain changes in different ways, but the exact mechanism by which most of these genes relate to the disease is still unknown.
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Neuroinflammation has gained increasing attention as a potential contributing factor in Alzheimer's disease (AD) pathology.
Why it matters
This study set out to test whether inflammatory proteins in cerebrospinal fluid could be useful for diagnosing Alzheimer's disease, noting that no such clinical biomarker has yet emerged. It screened for detectable proteins and examined their links to disease features and diagnostic accuracy, but the available text does not report a clear conclusion.
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Our results indicate that the inflammatory properties of circulating neutrophils shift as the percentage of aged neutrophils expands in patients with AD-changes that may play an instrumental role in establishing systemic chronic inflammation.
Why it matters
Blood samples from people with Alzheimer's dementia showed neutrophil hyperactivation and other changes in circulating neutrophils, and these abnormalities were greater in fast-decliners than slow-decliners. The authors say these changes may play a role in systemic chronic inflammation, but this is a description of what happens in the disease, not a treatment or cure.
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Additional study of mechanisms of action and methods for titrating stimulation parameters will be needed to determine if DBS has potential as an AD treatment.
Why it matters
In 42 participants with mild Alzheimer's disease, deep brain stimulation of the fornix had a favorable safety profile but showed no clinical benefits compared with delayed stimulation after one or two years. Post-hoc analyses suggested a possible benefit in participants over 65, but this was not a primary finding and requires further study.
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An increased HV:CTV ratio was predictive of faster clinical decline in participants with AD who were clinically indistinguishable at baseline except for a greater dysexecutive presentation.
Why it matters
Among amyloid-positive people with Alzheimer disease, those with a hippocampal-sparing pattern on MRI showed more Alzheimer-like hypometabolism and faster clinical decline than those with a limbic-predominant pattern. This is about using imaging subtypes to predict decline, not about treating, curing, or preventing the disease.
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Within the prospective population-based Rotterdam Study, we measured serum magnesium levels in 9,569 participants, free from dementia at baseline (1997-2008).
Why it matters
This study found that serum magnesium levels were associated with the risk of all-cause dementia and Alzheimer disease in a large population followed for years. It does not show that changing magnesium levels prevents or treats dementia, only that a link exists.
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Semantic-lexical retrieval and lexical search may represent distinct aspects of semantic memory.
Why it matters
In 42 women with mild-to-moderate Alzheimer disease, semantic memory scores were linked to global cognition, dementia severity, and daily function, and one factor predicted global cognition a year later. This suggests certain semantic memory tests may help track disease progression, though the analysis was small and secondary.
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Exposure to particulate matter (PM) in the ambient air and its interactions with APOE alleles may contribute to the acceleration of brain aging and the pathogenesis of Alzheimer's disease (AD).
Why it matters
In older US women from the WHIMS cohort, living where fine particulate air pollution exceeded EPA standards was associated with an 81% higher risk of global cognitive decline and a 92% higher risk of dementia, with stronger effects in women carrying two APOE ɛ4 copies. Separately, mice exposed to urban nanosized particles for 15 weeks developed more brain β-amyloid (worse with APOE ɛ4) and shrinkage of memory-region (CA1) nerve branches — the latter even in normal mice. The authors suggest air pollution may promote pathological brain aging; the human result is an association, not proof of cause.
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ADNI-3 will aim to inform AD treatment trials and facilitate development of AD disease-modifying treatments.
Why it matters
This paper lays out the plan for ADNI-3, a 5-year study that began on August 1, 2016 and follows people with normal cognition, mild cognitive impairment and Alzheimer's disease using tau imaging, brain-connectivity MRI and spinal-fluid tests, with amyloid PET "standardized using the Centiloid method." It describes methods, not results: its stated goal is "to validate biomarkers for Alzheimer's disease (AD) clinical trials" and to "inform AD treatment trials," and it reports no findings and tests no treatment.
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Genetic risk factors for Alzheimer's disease imply that inflammation plays a causal role in development of the disease.
Why it matters
Using post-mortem brain tissue from 299 participants, this study characterized microglial cell types in dementia with Alzheimer's pathology. It is an observational tissue study and does not test any treatment, so it cannot show whether targeting microglia would help patients.
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55/100
This longitudinal study sought to determine whether the 18 kDa translocator protein (TSPO), a marker of neuroinflammation, increases over time in Alzheimer's disease.
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55/100
Amyloid-positive cognitively healthy participants showed a significant increase in mI/creatine and mI/NAA levels compared to amyloid-negative healthy elderly (p Conclusions mI levels are elevated already at asymptomatic stages of AD.
Why it matters
This cross-sectional study found that a brain chemical called myo-inositol was already elevated in cognitively healthy people with abnormal amyloid, and also in healthy APOE ε4 carriers with normal amyloid. This suggests a possible early marker of Alzheimer disease, but it does not show any treatment or prevention.
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Using PET brain scans, researchers found that where tau protein tangles build up in the brain closely tracks which brain regions lose function and matches a person's specific symptoms (memory loss vs. language problems vs. visual problems), much more closely than where amyloid plaques sit.
Why it matters
Where tau tangles build up tracked local loss of brain glucose metabolism and matched each person's specific symptoms far more closely than where amyloid plaques sat. This supports tau location, rather than amyloid location, as the better explanation for why people with Alzheimer's have different symptoms.
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We developed an accurate prognostic model for predicting MCI-to-dementia progression over a three-year period.
Why it matters
This study developed a model using baseline data from 259 patients with mild cognitive impairment to predict progression to Alzheimer's dementia, with the best model combining cognitive and functional markers with MRI measures reaching 80% accuracy. Cognitive and functional markers were most predictive, while plasma proteomic markers had limited predictive utility, so this concerns prediction rather than treatment.
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Twelve studies were considered for analysis.
Why it matters
Pooling 12 studies with 13 535 patients with Alzheimer's and 22 976 healthy controls, this meta-analysis found that the TREM2 variant rs75932628 was linked to Alzheimer's in Caucasian populations. In East Asian populations, the authors conclude TREM2 variants are likely not associated with the disease, a reminder that genetic risk findings may not carry across ancestries.
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Similar to findings in adult mutation carriers, in the later preclinical and clinical stages of ADAD, mutation-carrying children were distinguished from control individuals by significantly higher plasma Aβ1-42 levels (mean [SD]: carriers, 18.8 [5.1] pg/mL and noncarriers, 13.1 [3.2] pg/mL; P Conclusions and relevance Children at genetic risk for ADAD have functional and structural brain changes and abnormal levels of plasma Aβ1-42.
Why it matters
In children carrying the PSEN1 E280A mutation, plasma Aβ1-42 levels were higher than in noncarriers, suggesting very early biomarker changes. This is a small cross-sectional study of the earliest changes and does not test any treatment, cure, or prevention.
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Even when adjusted for age at onset, symptom duration, and other demographic variables, APOEε2 is associated with milder AD pathology and less severe antemortem cognitive impairment compared to APOEε3 and ε4 alleles, suggesting a relative neuroprotective effect of APOEε2 in AD.
Why it matters
In this autopsy cohort study, the APOE ε2 allele was independently associated with lower Braak neurofibrillary tangle stages and possibly fewer neuritic plaques, while APOE ε4 was associated with more neuritic plaques and cerebral amyloid angiopathy. These findings help explain genetic effects on Alzheimer's disease pathology but do not provide a treatment, cure, or prevention.
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Our objective was to investigate cross-sectional associations between odor identification ability and imaging biomarkers of neurodegeneration and amyloid deposition in clinically normal (CN) elderly individuals, specifically testing the hypothesis that there may be an interaction between amyloid deposition and neurodegeneration in predicting odor identification dysfunction.
Why it matters
In 215 clinically normal elderly people, worse odor identification was associated with markers of neurodegeneration, and those with elevated cortical amyloid and thinner entorhinal cortex had worse odor identification. This cross-sectional study suggests a possible way to detect preclinical Alzheimer's disease and does not test any treatment, cure, or prevention.
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By fitting Cox proportional hazards models, we find that baseline model stage is a significant risk factor for conversion from both mild cognitive impairment to Alzheimer's disease (P = 2.06 × 10(-7)) and cognitively normal to mild cognitive impairment (P = 0.033).
Why it matters
A data-driven model found that a person's stage in a sequence of biomarker changes was a significant risk factor for progressing from mild cognitive impairment to Alzheimer's disease and from normal cognition to mild cognitive impairment. The model supports ideas about the order of biomarker changes but does not provide a treatment.
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55/100
Several potential disease-modifying drugs for Alzheimer's disease (AD) have failed to show any effect on disease progression in clinical trials, conceivably because the AD subjects are already too advanced to derive clinical benefit from treatment and because diagnosis based on clinical criteria alone introduces a high misdiagnosis rate.
Why it matters
This review discusses that low CSF amyloid-β1-42 together with high total tau and phosphorylated tau can predict progression to Alzheimer's dementia in people with mild cognitive impairment. It focuses on improving early diagnosis and standardizing these tests, not on treating or preventing the disease.
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The defining features of Alzheimer disease (AD) include conspicuous changes in both brain histology and behavior.
Why it matters
This 2014 review describes the two abnormal structures that define the Alzheimer's brain: amyloid plaques outside nerve cells, built from amyloid-β (a fragment of the amyloid precursor protein), and tangles inside them, built from tau. It states that symptoms "correlate with the accumulation of plaques and tangles" and are "a direct consequence of the damage and destruction of synapses that mediate memory and cognition". It presents no new data, and our record does not explain its title's idea of amyloid-β and tau as "the trigger and bullet", so treat that as the author's framing, not a tested result.
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The hippocampus is one of the earliest affected brain regions in Alzheimer's disease (AD) and its dysfunction is believed to underlie the core feature of the disease-memory impairment.
From across this topic
10 of the 5,172 studies in this topic, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
- Mapping the impact of age and APOE risk factors for late onset Alzheimer's disease on long range brain connections through multiscale bundle analysis
- Classifying and diagnosing Alzheimer’s disease with deep learning using 6735 brain MRI images
- Dementia with Lewy bodies and Alzheimer disease: neurodegenerative patterns characterized by DTI
- Translating genetic risk of Alzheimer's disease into mechanistic insight and drug targets
- Resilience in Black/African American Partner Caregivers of Persons With Alzheimer's Disease and Related Dementias
- Influence of Ibuprofen on glycerophospholipids and sphingolipids in context of Alzheimer´s Disease
- Molecular, Structural, and Functional Characterization of Alzheimer's Disease: Evidence for a Relationship between Default Activity, Amyloid, and Memory
- Physical and Cognitive Activities and Trajectories of AD Neuroimaging Biomarkers
- Revealing the nervous system requirements of Alzheimer disease risk genes in Drosophila
- Plasma d-glutamate levels for detecting mild cognitive impairment and Alzheimer's disease: Machine learning approaches