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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The amyloid precursor protein (APP) has been associated with Alzheimer's disease (AD) because APP is processed into the beta-peptide that accumulates in amyloid plaques, and APP gene mutations can cause early onset AD.
Why it matters
In lab-grown human astrocytes, the inflammatory signal interleukin-1 raised production of the amyloid precursor protein (APP) up to 6-fold (15-fold in astrocytoma cells) without changing APP mRNA levels. A 90-nucleotide stretch at the start of the APP message was enough to pass this control to an unrelated reporter gene. This suggests one way inflammation, which is raised in the Alzheimer's brain, could increase the protein that plaque-forming beta-peptide comes from. It is cell research and did not measure plaques or test any treatment.
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Neocortical neurofibrillary tangle densities were substantially correlated with dementia severity, and to a greater degree than was true for senile plaque densities.
Why it matters
This clinicopathologic study found that neocortical neurofibrillary tangle densities correlated with dementia severity more than senile plaque densities did. It describes brain pathology in relation to dementia severity, not a treatment, cure, or prevention.
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This report summarizes the consensus recommendations of a panel of neuropathologists from the United States and Europe to improve the postmortem diagnostic criteria for Alzheimer’s disease.
Why it matters
This report summarizes consensus recommendations from a panel of neuropathologists to improve postmortem diagnostic criteria for Alzheimer's disease. It is a diagnostic criteria paper and does not directly address treating, curing, or preventing Alzheimer's disease.
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In order to observe changes owing to aging and Alzheimer's disease (AD) in the volumes of subdivisions of the hippocampus and the number of neurons of the hippocampal formation, 18 normal brains from subjects who died of nonneurological causes and had no history of long-term illness or dementia (ten of these brains comprised the aged control group) and 13 AD brains were analyzed.
Why it matters
This brain tissue study found that the hippocampus was about 32% smaller in people with Alzheimer's disease than in controls, with neuron loss in specific regions, and that some shrinkage also occurred with normal aging. It supports using hippocampal volume in diagnosis but does not offer a treatment or cure.
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49/100
Magnetic resonance based volumetric measures of hippocampal formation, amygdala (A), caudate nucleus (CN), normalised for total intracranial volume (TIV), were analysed in relation to measures of cognitive deterioration and specific features of memory functions in 18 patients with probable Alzheimer's disease.
Why it matters
This study of 18 patients with probable Alzheimer's disease examined how MRI measures of the hippocampus and other brain regions related to memory test performance. It is a brain-imaging and memory study and does not test any treatment, cure, or prevention.
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This report summarizes the neuropathologic findings in the first 106 autopsies of CERAD (Consortium to Establish a Registry for Alzheimer's Disease) dementia patients diagnosed clinically as having Alzheimer's disease (AD).
Why it matters
This report summarizes neuropathologic findings in the first 106 autopsies of CERAD dementia patients diagnosed clinically as having Alzheimer's disease, with neuropathologists confirming Alzheimer's disease as the primary dementing illness in 92 cases. It addresses diagnostic confirmation and does not test a treatment, cure, or prevention.
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The apolipoprotein E4 (APOE4) allele is associated with an early age of onset of the nonfamilial form of Alzheimer disease (AD) and with increased beta protein amyloid deposition in the brain.
Why it matters
This laboratory study found that apoE3 slows the start of amyloid fibril formation in vitro, and that apoE4 is equally or slightly less able to do so. These are test-tube findings only and do not show that this can treat or prevent Alzheimer disease in people.
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The apolipoprotein E (apoE) type 4 allele (APOE4) is a susceptibility gene for late-onset familial and sporadic Alzheimer disease.
Why it matters
In this in vitro study, tau bound avidly to apoE3 but not to apoE4, and tau phosphorylated with a brain extract did not bind either isoform. The authors suggest that isoform-specific interactions of apoE with tau may regulate intraneuronal tau metabolism and alter the rate of formation of paired helical filaments and neurofibrillary tangles, but this is laboratory work with no demonstrated treatment, cure, or prevention.
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The Alzheimer A beta amyloid peptide (A beta) is the principal proteinaceous component of amyloid associated with Alzheimer disease (AD).
Why it matters
This study measured the relative amounts of different A beta variants in amyloid from the brains of people with sporadic Alzheimer's disease, familial Alzheimer's disease, and nondemented elderly controls. It describes the composition of amyloid but does not test or suggest any treatment, cure, or prevention.
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The clinical recognition of Pick's disease depends on its differentiation from Alzheimer's disease (AD).
Why it matters
Comparing 21 patients with pathologically confirmed Pick's disease and 42 with pathologically confirmed Alzheimer's disease, features such as presenile onset, initial personality change, hyperorality, disinhibition, and roaming behavior distinguished Pick patients. This concerns clinical differentiation, not treating, curing, or preventing Alzheimer's disease.
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In a double blind randomized crossover trial lasting 6 months selegiline, a selective MAO-B inhibitor, was tested against placebo for activity on verbal memory performances in Alzheimer-type dementia (DAT).
Why it matters
In a six-month double-blind crossover trial, selegiline showed significant activity on some verbal memory measures in people with Alzheimer-type dementia. The authors suggest this may reflect improved information processing and learning strategies during acquisition.
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Why it matters
Argues that amyloid deposition is the central event in the cause of Alzheimer's disease.
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Ninety-six individuals with Down syndrome over age 35 years were evaluated and followed up for evidence of nontreatable dementia.
Why it matters
Of 96 adults with Down syndrome over 35 who were followed, 49 developed dementia, at an average age of 54.2 years. In the 53 who lived in institutions, the share with dementia rose with age, from 2 of 25 (8%) at 35–49 to 11 of 20 (55%) at 50–59 and 6 of 8 (75%) over 60. Most of those with dementia (84%) developed seizures, and all 12 brains examined at autopsy showed plaques and tangles in the same locations as in Alzheimer's disease.
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Progressive cerebral deposition of extracellular filaments composed of the beta-amyloid protein (beta AP) is a constant feature of Alzheimer disease (AD).
Why it matters
This study identified the native beta-amyloid precursor protein as a 110- to 135-kDa membrane-associated protein complex in brain and other tissues. It provides basic information about the protein but does not test or suggest any treatment, cure, or prevention for Alzheimer's disease.
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Alzheimer's disease staging from structural magnetic resonance imaging (MRI) is challenging when clinically adjacent stages and severe class imbalance are considered simultaneously.
Why it matters
This study tested a computer model that sorts MRI brain scans into six stages, from cognitively normal to Alzheimer's disease, and it reached about 90% accuracy. However, scans from the same person could appear in both the training and test data, so the results show how well the model tells scans apart, not how well it would work on new patients.
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Thirty-three AD subjects, aged 69.3 ± 8.2 years (mean ± standard deviation), 18 females, and 22 HCs aged 70.5 ± 13.3 years, 15 females, were evaluated.
Why it matters
In 33 AD subjects and 22 healthy controls, a quantitative MRI measure called qT1 was higher in AD in several brain regions and was positively associated with amyloid PET. This small study supports qT1 mapping as a potential noninvasive imaging biomarker, not a treatment or cure.
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Individuals with autosomal dominant Alzheimer's disease (ADAD) arising from mutations in PSEN1, PSEN2, or APP exhibit variability in clinical presentation.
Why it matters
This genome-wide association study aimed to find genetic modifiers in people with mutations in PSEN1, PSEN2, or APP that cause autosomal dominant Alzheimer's disease. It may inform future therapeutic targets but does not itself report any treatment, cure, or prevention.
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We identified 8 brain structural features from 192 MRI features that were associated with the risk of MCI progressing to AD, including: left hippocampus, left inferior lateral ventricle, left amygdala, right middle temporal gyrus, left fusiform gyrus, right amygdala, left cortical total volume, and brain parenchyma total volume.
Why it matters
This longitudinal study identified several brain structural features and the APOE ε4 allele as independently associated with the risk of progression from mild cognitive impairment to Alzheimer's disease. It is about predicting progression and does not test any treatment, cure, or prevention.
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Latin America’s diverse genetic landscape provides a unique opportunity to study Alzheimer’s disease (AD) and frontotemporal dementia (FTD).
Why it matters
This first large-scale genetic study of Alzheimer's disease and frontotemporal dementia in Latin America identified pathogenic variants and families with autosomal dominant inheritance. It highlights the need to consider diverse ancestries and social factors when assessing genetic risk, but reports no treatment, cure or prevention.
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Presence of CHD may influence AD progression in DS.
Why it matters
In this matched study, adults with Down syndrome and congenital heart disease had higher amyloid burden and were projected to reach amyloid positivity at a younger age than those without congenital heart disease. The authors note the sample may be too young to show cognitive differences, and no treatment, cure or prevention was tested.
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Stroke interacts with APOE ε4 to influence dementia, with the association being more pronounced in APOE ε4 non‐carriers.
Why it matters
In this UK Biobank cohort of over 336,000 participants, both ischemic and hemorrhagic stroke were significantly associated with elevated risk of all-cause dementia and Alzheimer disease. The association of stroke with increased dementia risk was stronger in APOE ε4 non-carriers than carriers, with a significant interaction between stroke and APOE ε4.
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Our review supports that biofluid biomarker testing could be cost-effective to diagnose AD.
Why it matters
This review found that CSF biomarker tests were mostly cost-effective compared to neurocognitive assessments or neuroimaging, while blood biomarker tests showed mixed results. All included studies were model-based simulations rather than trial-based evaluations, so these findings rest on modelled assumptions about prevalence, diagnostic accuracy and treatment effectiveness.
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The study included 807 participants form K-ROAD (median age: 72.0 years, 58.7% female) and 230 from ADNI (median age: 70.9 years, 49.1% female).
Why it matters
A two-stage workflow combining MRI volume and plasma p-Tau217 improved diagnostic accuracy for predicting amyloid PET positivity in early-stage AD. The authors describe this as a cost-effective and scalable strategy for early detection, though they note some limitations.
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Subgroups with slower versus faster neurodegeneration, despite similar pathological accumulation, were compared to assess associations with genetic/lifestyles.
Why it matters
In dominantly inherited Alzheimer's disease, this study found that resistance was mainly linked to genetic mutations and physical activity, while resilience was influenced by modifiable lifestyle factors such as living arrangements and greater openness to experience. The findings suggest that lifestyle factors may help slow decline even when pathology accumulates, but this is an observational study in a specific inherited form of the disease and does not prove that any lifestyle change prevents or cures Alzheimer's disease.
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At 3 years, donanemab slowed disease progression on the Clinical Dementia Rating Scale (CDR)-Sum of Boxes (CDR-SB) in early-start participants versus a weighted ADNI control (-1.2 points; 95 % confidence interval [CI], -1.7, -0.7).
Why it matters
Over three years, donanemab slowed progression on a dementia rating scale in people with early symptomatic Alzheimer's disease compared with a weighted external control group. The trial also reported amyloid clearance and no new safety signals, but the comparison to an external control group is not the same as a randomized comparison.
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.
- Impaired lung function is associated with elevated blood biomarkers of AD/ADRD: unraveling the interplay with risk of dementia
- Dementia of Alzheimer's disease and other neurodegenerative disorders--memantine, a new hope
- Alzheimer's Disease Plasma Biomarkers Distinguish Clinical Diagnostic Groups in Memory Clinic Patients
- In vivo demonstration of Congo Red labeled amyloid plaques via perfusion in the Alzheimer disease rat model
- Global trends in Alzheimer’s disease and other dementias: A comprehensive analysis of incidence, socio-demographic variations, and future projections
- Added Value of Amyloid PET Quantification with the Centiloid Scale in Clinical Practice
- Alzheimer's disease: pathological mechanisms and the beneficial role of melatonin
- Choroid Plexus Volume and Permeability at Brain MRI within the Alzheimer Disease Clinical Spectrum
- Insulin-like growth factor-1 and risk of Alzheimer dementia and brain atrophy
- Self-Attention Augmented Wasserstein Generative Adversarial Network-based Detection of Brain Alzheimer Disease Using MRI