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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ALPS-index may provide useful disease progression or treatment biomarkers for patients with AD as an indicator of modulation of glymphatic activity.
Why it matters
In 50 participants, a measure of glymphatic system activity correlated negatively with amyloid and tau deposition on PET and positively with cognitive scores. The authors note this is an association and suggest the measure could serve as a progression or treatment biomarker, but the study does not show that altering glymphatic activity treats or prevents Alzheimer's.
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The proposed novel, pragmatic method to determine CSF biomarker cutoffs for AD does not require assessment of other biomarkers or assumptions concerning the clinical diagnosis of patients.
Why it matters
A new method for setting cutoff values for Alzheimer's spinal fluid biomarkers agreed closely with amyloid and tau PET imaging in one study group and was then applied to 10 large patient groups. This is a way to standardize diagnosis, not a treatment, cure or prevention.
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Well-authenticated biomarkers can provide critical insights into the biological basis of Alzheimer disease (AD) to enable timely and accurate diagnosis, estimate future burden and support therapeutic trials.
Why it matters
This review describes blood p-tau biomarkers as possible first-line diagnostic and prognostic tools that could allow wider population screening outside specialised centres. It discusses diagnostic and research use, not a treatment, cure or prevention.
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The ε4 allele of the apolipoprotein E gene (APOE4) is a strong genetic risk factor for Alzheimer's disease (AD) and several other neurodegenerative conditions, including Lewy body dementia (LBD).
Why it matters
This paper proposes an 'ApoE Cascade Hypothesis' in which the biochemical properties of apoE set off a cascade of cellular and systems events that lead to Alzheimer's disease and age-related cognitive decline. It predicts that apoE-targeted therapies may be more effective if aimed at the early biochemical phase, but this is a hypothesis, not a tested treatment or cure.
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58/100
Longitudinal racial differences in amyloid biomarkers are observed.
Why it matters
Among 179 Black and 1,180 White cognitively normal adults, amyloid biomarkers declined or accumulated more slowly in Black participants, and CSF total tau and phosphorylated tau181 increased about half as much. This is an observational study of biomarker differences and does not test any treatment or prevention for Alzheimer's disease.
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The current conceptualization of Alzheimer disease (AD) is driven by the amyloid hypothesis, in which a deterministic chain of events leads from amyloid deposition and then tau deposition to neurodegeneration and progressive cognitive impairment.
Why it matters
This paper proposes a revised 'probabilistic' model of Alzheimer's disease in which the amyloid cascade plays a smaller role in sporadic forms than in autosomal dominant forms, with random factors playing a larger role. The authors say this model could help guide research and the development of prevention and treatment strategies.
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CSF synaptic biomarkers increase in the early preclinical stages of the Alzheimer continuum even when a low burden of Aβ pathology is present, and they differ in their association with age, sex, APOE ε4 , and markers of neurodegeneration.
Why it matters
In middle-aged cognitively unimpaired participants, several CSF synaptic biomarkers increased with age and with higher amyloid load, even in people at the earliest preclinical stage. These are marker findings and do not show that any treatment, cure, or prevention works.
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These results indicate that trans-resveratrol has potential neuroprotective roles in the treatment of moderate to mild AD and that its mechanism may involve a reduction in the accumulation and toxicity of Aβ in the brain of patients, thereby reducing neuroinflammation.
Why it matters
In 30 patients with mild to moderate Alzheimer's disease, changes in blood and CSF Aβ40 with trans-resveratrol were not statistically significant, while the placebo group showed a significant decrease in Aβ40. This small study does not show that trans-resveratrol treats, cures, or prevents Alzheimer's disease.
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These findings suggest that DPP-4i use is associated with low amyloid burden and favorable long-term cognitive outcome in diabetic patients with ADCI.
Why it matters
In a review of 282 patients with diabetes and Alzheimer-related cognitive impairment, those taking DPP-4 inhibitors had lower amyloid burden on PET scans and a slower decline in MMSE scores than those not taking them. This is an observational association and does not prove that DPP-4 inhibitors treat or prevent Alzheimer's disease.
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Co-pathologies play an important role in the expression of the Alzheimer's disease clinical phenotype and may influence treatment efficacy.
Why it matters
This autopsy study compared the frequency of common neuropathological diagnoses in 96 patients with early-onset Alzheimer's disease and 48 with late-onset disease. It describes co-pathology and does not test any treatment.
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Three women (aged 61, 72, and 73 years) consecutively enrolled in the trial successfully completed repeated focused ultrasound-induced BBB opening of the hippocampus and entorhinal cortex.
Why it matters
In this small early trial, three women with early Alzheimer's disease safely underwent repeated focused ultrasound to open the blood-brain barrier in memory-related brain regions. The study only reports that the procedure was completed successfully and does not show whether it improves memory or changes the disease course.
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There were detectable WMH, enlarged PVS, infarcts, and microbleeds as early as the 5th decade of life.
Why it matters
In adults with Down syndrome, this cross-sectional study found signs of cerebrovascular disease on MRI as early as the fifth decade of life. It describes when these brain changes appear and how they relate to amyloid and cognitive status, but it does not test a treatment or prevention.
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Plasma markers have been reported to be associated with brain amyloid burden, tau pathology, or neurodegeneration.
Why it matters
This study used Alzheimer's Disease Neuroimaging Initiative data to test whether plasma biomarker profiles could predict Alzheimer's disease pathology and clinical progression in older adults without dementia. It is a cross-sectional and longitudinal observational study, so it cannot show that acting on these biomarkers would prevent or cure Alzheimer's disease.
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Four subphenotypes were computationally derived that correlated with cardiovascular diseases and mental health illnesses.
Why it matters
Using electronic health records and machine learning, this study derived four probable Alzheimer's disease subphenotypes and found prediction models showed promising results for predicting risk. It is about characterizing and predicting disease and does not report any treatment, cure, or prevention.
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Within APOE ε4 carriers, sex differences in CSF p-Tau are more evident in early disease stages, whereas for APOE ε4 noncarriers, sex differences are more evident in advanced disease stages.
Why it matters
Among 1,801 people with subjective cognitive decline, mild cognitive impairment or Alzheimer dementia, women had higher spinal-fluid tau levels than men, but where this showed up depended on APOE ε4. In ε4 carriers the difference was clearest at the early stages (SCD and MCI); in non-carriers it appeared at MCI and dementia but not SCD. This was a one-time comparison of groups, so it shows an association, not a cause, and it tests no treatment.
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This article describes the public health impact of Alzheimer's disease (AD), including incidence and prevalence, mortality and morbidity, use and costs of care, and the overall impact on caregivers and society.
Why it matters
This 2020 report pulls together US figures on Alzheimer's: an estimated 5.8 million Americans aged 65 and older had Alzheimer's dementia, a number it says "may grow to 13.8 million" by mid-century, and more than 16 million unpaid caregivers gave an estimated 18.6 billion hours of care valued at nearly $244 billion. Its special report says a shortage of dementia specialists is shifting care onto primary care doctors, many of whom "feel underprepared and inadequately trained". It is a descriptive report with estimates and projections, not a test of any treatment, and its figures are for the United States in 2018–2020.
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A faster termination of the stress response (higher coping ability) may limit the negative effects of stress on tau deposition.
Why it matters
Among 225 cognitively unimpaired older adults, better stress coping ability was associated with lower tau burden in several brain regions, with the link present in both amyloid-positive and amyloid-negative people but weaker in the latter. This is a cross-sectional association and does not show that improving coping treats, cures or prevents Alzheimer's disease.
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This study showed that plasma metabolites have the potential to match the AUC of well-established AD CSF biomarkers in a relatively small cohort.
Why it matters
This study used machine learning on blood metabolites to tell apart people with Alzheimer-type dementia from cognitively normal people, with accuracy similar to established CSF biomarkers. The authors say further studies in independent cohorts are needed to confirm whether this blood metabolite panel can separate Alzheimer's from controls and how specific it is for Alzheimer's compared with other neurodegenerative disorders.
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Multiple linear regression models identified sources of signal covariance between neuroinflammation and brain connectivity profiles, in relation to the diagnostic group (patients, controls) and cognitive status.
Why it matters
This study found that people with Alzheimer's disease had more neuroinflammation, and that stronger links between inflammation and abnormal brain connectivity went with worse cognitive deficits. It suggests future research into immunotherapy to slow progression, but no treatment was tested.
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Amyloid PET results were positive for 242 patients (48%).
Why it matters
Amyloid PET changed the suspected cause of symptoms in about a quarter of patients in a routine memory clinic, more often when the scan was negative than positive. This shows amyloid PET can affect diagnosis and treatment planning, but it does not show that it cures or prevents Alzheimer's disease.
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Although Aβ did not differ by sex, cognitive decline was greater in females with higher Aβ.
Why it matters
In 755 people without dementia (mean age 73.6) pooled from three research cohorts and followed for a median of 4 years, women and men had similar amyloid levels and APOE ε4 rates, and sex alone did not change how fast thinking scores declined. However, women with higher amyloid declined faster than men, and an exploratory (post hoc) analysis suggested the same for women who were both amyloid- and ε4-positive. The authors conclude sex "may play a modifying role" in Alzheimer's-related decline. This is an observational finding, and no treatment or prevention was tested.
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MeDi groups were comparable for clinical and neuropsychological measures.
Why it matters
In middle-aged adults without cognitive problems, lower adherence to a Mediterranean-style diet was associated with worsening Alzheimer-related brain imaging markers over three years. The authors call for further study of dietary interventions, so this does not yet show that diet prevents Alzheimer disease.
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These results suggest that, to optimize observing a treatment effect, clinical trials enrolling cognitively normal individuals should selectively recruit participants with abnormal levels of both amyloid and tau (ie, stage 2) because this group would be expected to show the greatest cognitive decline over time if untreated.
Why it matters
In 222 cognitively normal participants followed for a mean of 11 years, APOE ε4 genotype was not associated with baseline cognitive score or rate of cognitive change. The authors suggest that clinical trials should recruit participants with abnormal levels of both amyloid and tau to observe the greatest cognitive decline.
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58/100
Knight Alzheimer's Disease Research Center (ADRC) at Washington University (WU).
Why it matters
This study examined whether Alzheimer's disease biomarkers in spinal fluid and brain scans predict mood changes in cognitively normal older adults. It is about a possible link between biomarkers and mood, not about treating, curing or preventing the disease.
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A reliable method of detecting Alzheimer disease (AD) in its prodromal state is needed for patient stratification in clinical trials or for personalizing existing or potential upcoming therapies.
Why it matters
This cohort study combined plasma and cerebrospinal fluid information to improve prediction of progression from mild cognitive impairment to Alzheimer's dementia in 928 ADNI patients. It is about predicting progression for patient stratification, not treating, curing, or preventing the 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.
- Multi Layered Omics Approaches Reveal Glia Specific Alterations in Alzheimer's Disease: A Systematic Review and Future Prospects
- The role of magnetic resonance imaging in the diagnosis of Alzheimer disease in adults with Down syndrome
- Candidate Gene for the Chromosome 1 Familial Alzheimer's Disease Locus
- Astrocyte reactivity influences amyloid-β effects on tau pathology in preclinical Alzheimer's disease
- Cerebral infarctions and the likelihood of dementia from Alzheimer disease pathology
- β-Amyloid in Cerebrospinal Fluid: How to Keep It Floating (Not Sticking) by Standardization of Preanalytic Processes and Collection Tubes
- Type 2 Diabetes Interacts With Alzheimer Disease Risk Factors to Predict Functional Decline
- Seizures in Cerebral Amyloid Angiopathy
- Why do so many drugs for Alzheimer's disease fail in development? Time for new methods and new practices?
- APOE, vascular pathology, and the AD brain