Each study has a usefulness score out of 100 (rubric version 4.0). Tap a score to see what makes it up.
Highest usefulness score first. Studies without a score come last.
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Alzheimer's disease (AD) is a major form of senile dementia, characterized by progressive memory and neuronal loss combined with cognitive impairment.
Why it matters
This review describes five neuropathological hallmarks that have influenced Alzheimer's therapeutic approaches, including acetylcholine deficiency, glutamate excitotoxicity, amyloid-beta deposition, neurofibrillary tangles and neuroinflammation. It surveys drug candidates in clinical trials but reports no established cure or prevention.
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This study indicates that high AGE levels could be a contributing factor to impaired mobility but lacks evidence for an association with ADL decline in people with early stage AD or mixed dementia.
Why it matters
Following 144 people with early Alzheimer's or mixed dementia for a year, researchers found that higher levels of advanced glycation end products (AGEs) were associated with poorer mobility, but not with daily-living abilities. AGE levels rose and function declined over the year, though the change in AGEs did not track the change in mobility. The authors suggest AGEs may contribute to mobility problems and call for research on exercise, diet or drugs targeting AGE build-up.
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Accumulating evidence suggests that genetic variants in the SORL1 gene are associated with Alzheimer disease (AD), but a strategy to identify which variants are pathogenic is lacking.
Why it matters
This study developed a strategy to classify SORL1 gene variants as pathogenic or benign based on how damaging they are predicted to be and how rare they are. It found that strongly damaging, extremely rare SORL1 variants increased Alzheimer's risk by 12-fold, while more common SORL1 variants were not associated with increased risk.
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Higher gLFC connectivity is a functional substrate of CR that helps to maintain episodic memory relatively well in the face of emerging FDG-PET hypometabolism in early-stage AD.
Why it matters
In 44 patients with amnestic mild cognitive impairment who were amyloid-PET positive, higher global left frontal cortex connectivity was associated with more years of education and weakened the link between precuneus hypometabolism and lower memory performance. This concerns cognitive reserve, not treating, curing or preventing Alzheimer disease.
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The gut microbiota comprises a complex community of microorganism species that resides in our gastrointestinal ecosystem and whose alterations influence not only various gut disorders but also central nervous system disorders such as Alzheimer's disease (AD).
Why it matters
This review describes how the gut microbiota may influence Alzheimer's disease through the microbiota-gut-brain axis, including effects on gut and blood-brain barrier permeability and inflammation. It reports findings from animal studies and suggests a possible role, not a treatment, cure, or prevention.
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Neuropsychiatric symptoms are common manifestations of Alzheimer's disease (AD).
Why it matters
This preliminary study looked at risk factors and brain pathology in people with autopsy-confirmed Alzheimer's disease who had agitation or aggression. It does not test any treatment or prevention, and its findings are early and need confirmation.
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Alzheimer disease (AD) pathology starts long before clinical symptoms manifest, and there is no therapy to treat, delay, or prevent the disease.
Why it matters
This preclinical work tested whether young blood plasma could help in a mouse model of Alzheimer's disease, since young plasma had shown benefits on synaptic function and behavior in old mice. It is early animal research and does not establish any treatment, cure or prevention for people.
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Intracellular inclusions consisting of TAR DNA binding protein-43 (TDP-43 pathology) are present in up to 57% of Alzheimer's disease (AD) cases and follow a distinct topographical pattern of progression described in the TDP-43 in AD staging scheme.
Why it matters
This post-mortem brain study measured how common and severe TDP-43 pathology is in Alzheimer's disease, dementia with Lewy bodies, mixed cases and aged controls. It describes disease pathology only and offers no treatment, cure or prevention.
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Age, apolipoprotein E ε4 (APOE) and chromosomal sex are well-established risk factors for late-onset Alzheimer's disease (LOAD; AD).
Why it matters
This review discusses how age, APOE-ε4 and chromosomal sex interact as risk factors for late-onset Alzheimer's disease, with APOE-ε4 risk appearing greater in women and a specific risk in APOE-ε4 positive men. It argues for a precision medicine approach but reports no treatment, cure or prevention.
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Genome-wide association studies have identified rare variants of the gene that encodes triggering receptor expressed on myeloid cells 2 (TREM2) - an immune receptor that is found in brain microglia - as risk factors for non-familial Alzheimer disease (AD).
Why it matters
Genetic studies had linked rare variants of TREM2, an immune receptor on the brain's microglia, to a higher risk of non-familial Alzheimer's, and animal studies suggested these variants may change how microglia react to amyloid plaques. This 2016 review explores how TREM2 may control that response, its possible role in microglial ageing, its interactions with proteins made by other Alzheimer's risk genes, and the "hypothetical consequences" of TREM2 being cut from the cell surface. It reports no new data and proposes ideas to test, not a treatment.
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This study provides evidence for heterogeneous pathologic substrates and possibly different pathophysiologic mechanisms underlying MRI-observed cortical microbleeds in the context of advanced CAA and Alzheimer disease.
Why it matters
This small autopsy study found that microbleeds seen on MRI in people with severe cerebral amyloid angiopathy and Alzheimer pathology had heterogeneous causes, including recent hemorrhage, vasculopathy, and old hemorrhage with ischemic injury. It helps explain what these MRI findings represent, but it does not test a treatment, cure, or prevention.
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Alzheimer's disease is the most common type of dementia, and it is characterized by a decline in memory or other thinking skills.
Why it matters
This article notes that advanced age is the greatest risk factor for Alzheimer's disease and that a genome-wide study identified a locus on chromosome 17 associated with age at onset, with a specific variant in CCL11 probably responsible. It suggests that a protective haplotype associated with a 10-year delay in onset might allow future development of immunomodulators with the potential to halve disease incidence.
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We recently demonstrated that the frequencies of biomarker groups defined by the presence or absence of both amyloidosis (A+) and neurodegeneration (N+) changed dramatically by age in cognitively non-impaired subjects.
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Determination of sensitive and specific markers of very early AD progression is intended to aid researchers and clinicians to develop new treatments and monitor their effectiveness, as well as to lessen the time and cost of clinical trials.
Why it matters
A machine learning algorithm using MRI scans classified Alzheimer's disease versus healthy controls with 76% accuracy, and MCI patients who converted to Alzheimer's versus those who did not with 66% accuracy. This is a diagnostic tool study, not a treatment trial, so it does not show that any treatment, cure, or prevention works.
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Hippocampal atrophy, as evidenced using magnetic resonance imaging (MRI), is one of the most validated, easily accessible and widely used biomarkers of Alzheimer's disease (AD).
Why it matters
This 2015 review reports that "most studies" found shrinkage concentrated in one part of the hippocampus, the CA1 subfield, in early Alzheimer's disease, before it spreads more widely at the dementia stage. "Preliminary studies" suggested that looking at this pattern, rather than the whole hippocampus, improves diagnostic accuracy at the mild cognitive impairment stage. The authors add that methods vary widely between studies and that standardised protocols and larger samples are needed "to confirm the clinical utility of these techniques". It is about diagnosis, not treatment.
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Recent studies show that heterozygous variant of triggering receptor expressed on myeloid cells 2 (TREM2) increase the risk of Alzheimer's disease (AD) but with inconclusive results.
Why it matters
This meta-analysis found that three TREM2 variants were linked to higher Alzheimer's risk, with rs75932628 showing an odds ratio of 2.70. The authors caution that results for rs104894002 and rs143332484 were less robust and need larger, more diverse samples. They conclude TREM2 is a candidate gene for Alzheimer's susceptibility.
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Analysis of variances, adjusted for sex and age, showed that all structures, except the globus pallidus, were smaller in AD than in controls.
Why it matters
In 773 participants, loss of subcortical grey matter volume, including the nucleus accumbens in addition to the hippocampus, was associated with conversion from mild cognitive impairment to Alzheimer's disease. This supports using brain imaging to identify those at higher risk, but no treatment was tested.
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The clinical symptoms of Alzheimer disease (AD) include a gradual memory loss and subsequent dementia, and neuropathological deposition of senile plaques and neurofibrillary tangles.
Why it matters
In post-mortem brain tissue, altered mTOR signaling and reduced autophagy were found at early stages of Alzheimer's disease, including preclinical and amnestic mild cognitive impairment. This suggests these changes occur early in the disease process, but it does not show that targeting them treats or prevents Alzheimer's disease.
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Spatially distinct neurodegeneration is associated with Aβ and tau pathology in preclinical AD.
Why it matters
In 188 cognitively normal older individuals, elevated CSF tau was associated with cortical thinning in Alzheimer disease signature regions but not hippocampal atrophy, while decreased CSF β-amyloid 42 was associated with hippocampal loss but not cortical thinning. This describes how two pathologies relate to different brain changes in preclinical Alzheimer's disease, not a treatment or cure.
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Biomarkers in the cerebrospinal fluid (CSF) can track specific pathophysiological pathways underlying Alzheimer's disease (AD).
Why it matters
This study measured six cerebrospinal fluid markers of amyloid processing, neuronal damage, and inflammation in a clinical cohort with different neurodegenerative conditions to explore how these markers relate to each other. It is a biomarker study and does not test any treatment, cure, or prevention.
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Hippocampal sclerosis of aging (HS-Aging) neuropathology was observed in more than 15% of aged individuals in prior studies.
Why it matters
This study analyzed autopsy data to describe the clinical and pathological features linked to hippocampal sclerosis of aging and how it compares with Alzheimer's disease and frontotemporal lobar degeneration. It is a pathology study and does not test any treatment, cure, or prevention.
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Concordance between scan results and baseline diagnosis was high (PiB 84%, FDG 82%).
Why it matters
At one academic dementia center, amyloid (PiB) PET scans agreed with doctors' pre-scan diagnosis in 84% of 140 patients, and the diagnosis changed afterwards in 9% (13/140) — rising to 38% (5/13) among patients whose diagnosis was unclear beforehand. The authors found amyloid PET changed thinking more than FDG-PET, and changed diagnoses more than treatment plans, calling the overall effect "moderate". The study looked back at research patients, so the authors say prospective studies are needed; it does not show that scanning improves patient outcomes.
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This study evaluates the individual, as well as relative and joint value of indices obtained from magnetic resonance imaging (MRI) patterns of brain atrophy (quantified by the SPARE-AD index), cerebrospinal fluid (CSF) biomarkers, APOE genotype, and cognitive performance (ADAS-Cog) in progression from mild cognitive impairment (MCI) to Alzheimer's disease (AD) within a variable follow-up period up to 6 years, using data from the Alzheimer's Disease Neuroimaging Initiative-1 (ADNI-1).
Why it matters
In 381 people with mild cognitive impairment from the ADNI-1 study, followed for up to 6 years, an MRI score of brain-shrinkage patterns (SPARE-AD) and a memory-and-thinking test (ADAS-Cog) predicted who progressed to Alzheimer's about equally well, and together they predicted better than either alone. Adding APOE genotype, or spinal-fluid amyloid and tau markers (tested in 192 of them), did not significantly improve prediction. The MRI score also predicted progression in people without amyloid build-up, which the authors call unexpected and say needs further study. This is a prediction study, not a treatment.
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The cause and mechanism of development of Alzheimer' s disease (AD) remain unexplained.
Why it matters
Drawing on a meta-analysis of published studies, this review argues that the raised cortisol (a stress hormone) seen at mild-to-moderate Alzheimer's stages follows a specific daily rhythm, unlike the constantly high levels in Cushing's disease or major depression. The author proposes that this pattern may help start sporadic Alzheimer's and that neuroinflammation later suppresses glucocorticoid receptor signalling. These are theoretical proposals that the author says merit further scrutiny, not tested findings.
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SUVr(60-90) and SUVr(40-60) overestimated binding with 13% and 10%, respectively, compared with RPM2.
Why it matters
This methods study compared ways of measuring amyloid PET changes over time and found that some common methods overestimate binding. It is about how to reliably measure amyloid in drug studies, not about a treatment itself.
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.
- 2003-2013: a decade of body mass index, Alzheimer's disease, and dementia
- Detection of Alzheimer Disease Pathology in Patients Using Biochemical Biomarkers: Prospects and Challenges for Use in Clinical Practice
- Quantifying Uncertainty in Alzheimer's Disease Progression Modelling: A Variational Disease Progression Score Framework
- Functional and Phenotypic Diversity of Microglia: Implication for Microglia-Based Therapies for Alzheimer's Disease
- An epidemiological study of Alzheimer's disease in elderly Mongolian and Han populations living in rural areas of Inner Mongolia
- Emerging trends in Alzheimer's disease diagnosis and prediction using artificial intelligence: A bibliometric analysis of the top cited 100 articles
- Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer's disease
- Mapping distributed sources of cortical rhythms in mild Alzheimer's disease. A multicentric EEG study
- Valacyclovir Treatment of Early Symptomatic Alzheimer Disease: The VALAD Randomized Clinical Trial
- Comparison of Plasma p-tau217 and [18F]FDG-PET for Identifying Alzheimer Disease in People With Early-Onset or Atypical Dementia