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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There is overwhelming evidence to suggest that the neuropathology of Alzheimer disease (AD) extends beyond amyloid plaques and neurofibrillary tangles.
Why it matters
This review states that more than 30% of Alzheimer's disease cases show cerebrovascular pathology, and that about one third of patients diagnosed with vascular dementia have Alzheimer's-type pathology at autopsy. It considers whether these vascular lesions are coincidental or causal in the disease process, which remains to be defined.
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Amyloid precursor protein (APP) plays a central role in Alzheimer disease.
Why it matters
This study describes the crystal structure of a part of the amyloid precursor protein, noting that the protein's normal function is still largely unknown. It provides structural information only and does not test any treatment, cure, or prevention.
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44/100
The ideal biomarker for Alzheimer’s disease (AD) should detect a fundamental feature of neuropathology and be validated in neuropathologically-confirmed cases; it should have a sensitivity >80% for detecting AD and a specificity of >80% for distinguishing other dementias; it should be reliable, reproducible, non-invasive, simple to perform, and inexpensive.
Why it matters
A working group stated that an ideal Alzheimer's biomarker should have a sensitivity above 80% for detecting the disease and a specificity above 80% for distinguishing other dementias, and be reliable, non-invasive, simple and inexpensive. Of the candidates reviewed, low cerebrospinal fluid levels of Aβ42 and high levels of tau came closest to meeting the criteria for sporadic Alzheimer's.
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Cerebral plaques containing beta-amyloid (beta A4) represent an invariant pathological feature of Alzheimer disease (AD). beta A4 is proteolytically generated from its parent molecule, amyloid precursor protein (APP).
Why it matters
Using cultured hippocampal neurons, this study found that intracellular and secreted amyloid-beta species are generated by distinct mechanisms. This is cell-based work and does not test any treatment or show how to prevent Alzheimer's disease.
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Sixteen affected individuals are described from two families with early onset autosomal dominant familial Alzheimer's disease.
Why it matters
This study describes two families with an inherited form of early-onset Alzheimer's disease caused by a specific presenilin 1 gene mutation, and found that age at onset clustered within each family but differed between families, suggesting another genetic factor affects when the disease starts. It is a description of 16 affected individuals and does not test any treatment or prevention.
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This article reports the development and psychometric properties of the Alzheimer's Disease Cooperative Study-Clinical Global Impression of Change (ADCS-CGIC).
Why it matters
Reports the development and testing of the ADCS-CGIC, a clinician rating of overall change designed for Alzheimer's clinical trials. At 12 months, 81% of untreated Alzheimer's participants were rated as worsened, while only 2% of controls showed minimal worsening, and the authors conclude it is valid and reliable for use in clinical trials.
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A key pathological feature of Alzheimer's disease (AD) is the formation and accumulation of amyloid fibers within the neurophil as senile plaques and in the walls of cerebral and meningeal blood vessels.
Why it matters
This laboratory study examines how substituting charged residues affects the conformation and fiber formation of amyloid-beta peptides. It is basic chemistry work and does not test or establish any treatment, cure, or prevention for Alzheimer's disease.
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BANS-S may be a useful tool for the evaluation of different treatment strategies in severe DAT and for the correlation of clinical and pathological findings.
Why it matters
A new scale (BANS-S) was developed to measure severity in advanced Alzheimer's disease when other scales lose sensitivity, and its scores correlated with brain pathology after death. This is a measurement tool for evaluating treatments in severe disease, not a treatment itself.
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44/100
Recent data have demonstrated genetic disequilibrium between inheritance of the apolipoprotein E (apoE) epsilon 4 allele and increased risk of Alzheimer disease.
Why it matters
In a large clinic-based population, this study confirmed that inheriting the APOE4 allele is linked to a higher risk of Alzheimer's disease. It also reported that inheriting the APOE2 variant is negatively associated with the risk of developing Alzheimer's disease.
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Using magnetic resonance imaging (MRI), we measured the volumes of various brain structures and cerebrospinal fluid (CSF) in 19 men with dementia of the Alzheimer type (DAT) and 18 healthy age-matched control men.
Why it matters
In 19 men with dementia of the Alzheimer type, brain matter and temporal lobe volumes were significantly smaller and ventricular and temporal lobe CSF volumes larger than in controls, with temporal lobe loss greater than whole brain loss. These are structural correlations with disease severity and do not test any treatment or cure.
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Amyloid plaque cores were purified from Alzheimer disease brain tissue.
Why it matters
This study purified and analyzed amyloid plaque core proteins from Alzheimer's disease brain tissue, identifying several components. It is basic biochemical characterization and does not test any treatment, cure or prevention.
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The Alzheimer beta/A4 amyloid precursor protein (APP) can be proteolytically processed by at least two separate pathways in PC12 cells: chloroquine-insensitive secretory cleavage and chloroquine-sensitive intracellular degradation, presumably in the endosomal/lysosomal system.
Why it matters
This laboratory work in PC12 cells found the amyloid precursor protein inside clathrin-coated vesicles, which carry proteins to the endosomal compartment. It is early cell-based research about how amyloid precursor protein is processed and does not show any treatment, cure or prevention for Alzheimer's disease.
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Cells of the mononuclear phagocytic system (MPS) present foreign antigen on their cell surfaces bound to major histocompatibility complex (MHC) class II molecules.
Why it matters
This study describes increased MHC class II-expressing microglia in Alzheimer's disease and a close physical association between these cells and senile plaque beta-amyloid. It is a descriptive tissue study and does not test any treatment or prevention.
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44/100
We have recently shown that the amyloid beta A4 precursor protein (APP) is synthesized in neurons and undergoes fast axonal transport to synaptic sites [Koo et al., Proc.
Why it matters
This study found that the amyloid precursor protein is located at synapses in human and rat brain and at neuromuscular junctions. That location suggests the protein has a normal role in synaptic activity and that synapses could be affected early in Alzheimer's disease, but the work describes localization only and does not test any treatment.
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The amyloid forming beta-peptide of Alzheimer's disease is synthesized as part of a larger integral membrane precursor protein (beta APP) of which three alternatively spliced versions of 695, 751, and 770 amino acids have been described.
Why it matters
This laboratory work describes how the amyloid precursor protein is processed and identifies a stable intermediate fragment that remains in cells. It does not test any treatment or show how to prevent or cure Alzheimer's disease.
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Cells expressing leucocyte common antigen (LCA) as well as T-cytotoxic-suppressor (T8) and T-helper-inducer (T4) antigens were detected in significant numbers in the hippocampus and temporal cortex of Alzheimer but not normal brain tissue.
Why it matters
This study detected cells expressing leucocyte common antigen and T-cytotoxic-suppressor and T-helper-inducer antigens in Alzheimer's disease brain tissue but not normal brain tissue, indicating an immunocompetent status of microglia. It is a descriptive tissue finding and provides no treatment, cure or prevention.
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The neuropathology of Down syndrome (DS) at middle age is compared with that of Alzheimer disease (AD) at that age, through a review of the published literature and from the author's personal observations on brains from a series of patients of different ages with DS.
Why it matters
By comparing brains from people with Down syndrome with published descriptions of Alzheimer's disease, this 1988 paper found that plaques, tangles and the pattern of brain shrinkage at middle age are "qualitatively the same" in both conditions, though "quantitative differences do occur." It concluded that "in pathological terms" people with Down syndrome at middle age "do indeed have" Alzheimer's disease. This finding describes brain tissue after death, not memory or dementia symptoms, and the summary gives no sample size and tests no treatment.
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Hereditary cerebral hemorrhage with amyloidosis in Dutch patients is an autosomal dominant form of vascular amyloidosis restricted to the leptomeninges and cerebral cortex.
Why it matters
This small study of five patients found that the vascular amyloid in this inherited bleeding disorder reacts with an antiserum against the Alzheimer-related beta-protein, suggesting the two conditions share a disease mechanism. It supports the idea that amyloid builds up in blood vessel walls before damaging brain tissue, but it does not test any treatment or cure.
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Cognitive impairment is an important non-motor manifestation of amyotrophic lateral sclerosis (ALS), particularly across the ALS-frontotemporal dementia (ALS-FTD) spectrum.
Why it matters
This systematic narrative review and evidence map examined whether cerebrospinal fluid tau and amyloid biomarkers reflect cognitive impairment across the ALS-FTD spectrum, and found the available evidence limited, fragmented, and methodologically heterogeneous. It identifies gaps in biomarker knowledge and does not provide a treatment, cure, or prevention for Alzheimer's disease.
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43/100
Damaging nonsynonymous ABCA1 variants had differential AD risk effects between APOE genotype groups and exhibited interaction effects with APOE ε2 and ε4.
Why it matters
This study found that damaging nonsynonymous ABCA1 variants had differential Alzheimer disease risk effects between APOE genotype groups and interacted with APOE ε2 and ε4. Predicted ABCA1 activity based on HDL-associated variants was associated with reduced Alzheimer disease risk and interacted with APOE ε4, though replication analyses were not statistically significant in the APOE interaction model.
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The machine learning model predicted MMSE scores with a root-mean-squared error (RMSE) of 2.43 in the BH test set.
Why it matters
A machine learning model using a digital clock and recall test predicted MMSE scores with reasonable accuracy, which could help streamline eligibility assessment for Alzheimer's disease-modifying therapies. This is a tool for assessment, not a treatment or prevention for the disease itself.
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CSF samples were retrospectively collected from 253 subjects recruited at Peking Union Medical College Hospital, Xuanwu Hospital Capital Medical University, and Beijing Tiantan Hospital between July 2013 and September 2019.
Why it matters
Using cerebrospinal fluid from 253 subjects, this study evaluated whether a domestic Lifotronic platform, a Japanese LUMIPULSE platform, and an American Meso Scale Discovery platform gave consistent results for core Alzheimer's disease cerebrospinal fluid biomarkers. It is a measurement comparison and does not test treatment, cure, or prevention.
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The MMSE–CDR‐SB residual may help flag less AD‐typical presentations for further etiologic evaluation, but cannot be interpreted as a pathology‐specific marker due to substantial overlap across diagnostic groups.
Why it matters
A measure called the MMSE–CDR-SB residual, based on how much a person's daily functioning differs from what their cognitive score would predict, was linked to different underlying brain pathologies at autopsy. This is an exploratory diagnostic indicator and does not test any treatment or prevention.
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The Hierarchical-Circular Model of Biological Memory offers a unifying hypothesis for Alzheimer's disease and related dementias that bridges genetic, epigenetic, physiological, neuroimmune, and interoceptive processes across the lifespan.
Why it matters
This is a conceptual hypothesis, not a test of any treatment, so it does not show that anything cures or prevents Alzheimer's disease. It proposes a framework to guide future research into prevention and personalized treatment.
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VBPs indicate how much 174 countries should be willing to pay.
Why it matters
This modelling study estimated value-based prices for lecanemab and donanemab across 174 countries based on cost-effectiveness and country-level thresholds, with lecanemab and donanemab increasing average QALYs by 0.38 and 0.51 respectively compared with usual care. It addresses how much countries should be willing to pay and does not itself establish that these therapies cure or prevent Alzheimer's disease.
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.
- Alzheimer blood biomarkers: practical guidelines for study design, sample collection, processing, biobanking, measurement and result reporting
- Multi-ancestry genome-wide meta-analysis of 56,241 individuals identifies known and novel cross-population and ancestry-specific associations as novel risk loci for Alzheimer's disease
- Clinical and Biomarker Changes in Dominantly Inherited Alzheimer's Disease
- Plasma amyloid, tau, and neurodegeneration biomarker profiles predict Alzheimer's disease pathology and clinical progression in older adults without dementia
- Increased Prevalence in Alzheimer Disease in the Northeast Tennessee Region of the United States
- The views of Alzheimer disease patients and their study partners on proxy consent for clinical trial enrollment
- Associations Between Tau, β-Amyloid, and Cognition in Parkinson Disease
- Beta-amyloid precursor protein of Alzheimer disease occurs as 110- to 135-kilodalton membrane-associated proteins in neural and nonneural tissues
- Cotton wool plaques in non-familial late-onset Alzheimer disease
- Diagnostic and Prognostic Utility of the Synaptic Marker Neurogranin in Alzheimer Disease