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 5,413 studies, highest score first: BibTeX (.bib) · RIS (.ris)
Highest usefulness score first. Studies without a score come last.
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66/100
The APOE epsilon4 allele is a genetic risk factor for dementia with stroke, including VaD and AD with CVD.
Why it matters
In this population-based case-control study, people with dementia and stroke were more likely to carry the APOE epsilon4 allele, with homozygotes having about a 7-fold increased risk. This describes a risk factor for dementia with stroke, not a treatment, cure or prevention.
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Subjective cognitive decline (SCD) is proposed as an indicator of transitional disease stage 2 in the Alzheimer's disease (AD) continuum.
Why it matters
In 457 participants, elevated and faster-rising plasma p181 levels in amyloid-positive individuals with subjective cognitive decline predicted cognitive decline and transition to mild cognitive impairment. This is a biomarker study supporting staging and risk identification, not a test of any treatment, cure, or prevention for Alzheimer's disease.
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Evidence regarding the clinical validity of blood biomarkers of Alzheimer's disease (AD) in the general population is limited.
Why it matters
In 2,148 dementia-free older adults in Sweden followed for up to 16 years, higher blood levels of p-tau181, p-tau217, NfL and GFAP were linked to higher risk of all-cause and Alzheimer's dementia. Over 10 years, a negative result was reassuring (negative predictive value above 90%), but a positive one was not: even the best pairing, p-tau217 with NfL or GFAP, had a positive predictive value of only 43%. The authors conclude that these tests may help rule out impending dementia, but probably need to be combined with other biological or clinical markers before they can be used for screening.
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The genetic component of early-onset Alzheimer disease (EOAD), accounting for ~10% of all Alzheimer's disease (AD) cases, is largely unexplained.
Why it matters
This genetic analysis found shared genetic factors between early-onset Alzheimer disease and blood lipid traits, identifying overlapping loci including APOE and TREM2. It suggests that lipid pathways may be involved in early-onset Alzheimer disease, but no treatment or prevention is tested.
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65/100
Alzheimer's disease (AD) therapies utilizing amyloid-β (Aβ) immunization have shown potential in clinical trials.
Why it matters
Using spatial transcriptomics in human brain tissue, this study identified distinct microglial states associated with amyloid-beta clearance and found upregulation of TREM2 and APOE in microglia across immunization approaches, correlating with antibody responses and amyloid-beta removal. These findings describe mechanisms seen in immunized patients and point to possible molecular targets, but they do not show that targeting them treats or prevents Alzheimer's disease.
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This study classified preclinical Alzheimer's disease (AD) using cognitive screening, neighborhood deprivation via the area deprivation index (ADI), and sociodemographic and genetic risk factors.
Why it matters
Using cognitive screening, neighborhood disadvantage, and genetic and social factors, machine learning models slightly improved prediction of preclinical Alzheimer's disease, with a combined model performing best. This is about early detection, not treatment or cure, and the improvement from neighborhood factors was described as slight.
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Among the plasma biomarkers, phosphorylated tau (p-tau) 217 exhibited the highest concordance rate with Aβ (2326 of 2571 [90.5%]) and tau (100 of 120 [83.3%]) PET.
Why it matters
This study compared blood biomarker results with PET scans and found that p-tau217 matched amyloid and tau PET results most often, while some people had mismatched results. It is about interpreting biomarker tests, not about treating, curing, or preventing Alzheimer's disease.
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These results suggest that AADvac1 tau immunotherapy can reduce plasma biomarkers of neurodegeneration and neuroinflammation.
Why it matters
In a later look at the ADAMANT trial, 137 of 196 participants with mild Alzheimer's had high blood p-tau217, and in this group the tau vaccine AADvac1 was safe and well tolerated. It reduced the build-up of the blood markers NfL by 56% and GFAP by 73%, but its edge on thinking and daily-living scores was not statistically significant. The authors call these results hypothesis-generating and say a larger trial is needed.
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Alzheimer's disease (AD) is the leading cause of dementia in older adults.
Why it matters
This cell atlas study of the middle temporal gyrus in donors with varying Alzheimer's disease pathologies revealed two disease phases: an early phase with slow pathology increase, inflammatory microglia, reactive astrocytes, loss of somatostatin+ inhibitory neurons, and a remyelination response; and a later phase with exponential pathology increase and loss of excitatory neurons and Pvalb+ and Vip+ inhibitory neuron subtypes. These findings were replicated in other major Alzheimer's disease studies.
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This study validated PrecivityAD2, a mass-spectrometry blood test made by C2N Diagnostics that combines two markers (%p-tau217 and the amyloid-beta 42/40 ratio) into a single 'Amyloid Probability Score 2.'
Why it matters
A blood test can reliably detect amyloid protein in the brain, which is associated with Alzheimer's pathology, by measuring %p-tau217 and the amyloid-beta 42/40 ratio. This validation study in 583 people shows the blood test agrees with brain imaging about 88% of the time, but does not demonstrate whether using this test to guide treatment decisions improves outcomes.
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65/100
The use of an amyloid clock enabled visualization and analysis of biomarker changes as a function of estimated years from symptom onset in sporadic AD.
Why it matters
Using an amyloid clock, this study estimated that several blood and cerebrospinal fluid biomarkers change many years before estimated symptom onset in sporadic Alzheimer's disease. This is about timing of biomarker changes, not about treating, curing or preventing the disease.
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The advent of proteomics offers an unprecedented opportunity to predict dementia onset.
Why it matters
Following 52,645 dementia-free UK Biobank adults for 14.1 years (1,417 developed dementia), researchers measured 1,463 blood proteins and found GFAP, NEFL, GDF15 and LTBP2 most consistently linked to later all-cause dementia, Alzheimer's disease and vascular dementia, with GFAP and NEFL changing at least 10 years before diagnosis. GFAP (or GDF15) combined with demographic information predicted all-cause dementia with an AUC of 0.891 and Alzheimer's with 0.872, and people with higher GFAP were 2.32 times more likely to develop dementia. The authors see this as pointing toward blood-based screening of high-risk people, but it is a prediction study of associations, not a test of any treatment.
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This study tracked tau PET scans over time in over 800 people across the Alzheimer's spectrum and found that while tau broadly follows the classic 'Braak stage' spreading pattern, the exact regions affected vary a lot from person to person, especially as disease progresses.
Why it matters
Tau generally followed the expected Braak spreading order, but which exact regions were affected varied a lot between people, and tau spread fastest in the mild cognitive impairment stage. This suggests treatments aimed at tau may need to account for individual differences in where it spreads, especially early on.
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There were no statistical differences between the placebo or solanezumab groups in CDR-G, CDR-SB, specific CDR boxes or CDR composite scores over the course of the trial.
Why it matters
In this study of cognitively unimpaired older people with brain amyloid, there were no statistical differences between the placebo and solanezumab groups on cognitive and functional measures over the trial. It suggests that specific clinical rating scale changes may help measure expected treatment effects in future prevention trials, but it shows no benefit from solanezumab.
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In patients with Alzheimer's disease pathophysiological changes of the brain that initiate the onset of Alzheimer's disease include accumulation of amyloid-β plaques and phosphorylation of tau-tangles.
Why it matters
Of 1962 studies assessed, 17 showed possible links between oral diseases and Alzheimer's, and the authors grouped the proposed explanations into 4 theories involving germs, inflammatory signals, APOE gene variants and Aβ. Inflammation caused by poor oral health was the common thread. However, the review found the evidence insufficient to prove a link, so better dental care as a way to prevent decline remains an idea for future research.
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65/100
In this study, patients with Alzheimer dementia who took brexpiprazole, 2 or 3 mg, showed a statistically significant improvement vs placebo in agitation over 12 weeks.
Why it matters
In this trial of 345 patients, those taking brexpiprazole 2 or 3 mg showed statistically significantly greater improvement in agitation than those taking placebo over 12 weeks. This addresses a behavioral symptom of Alzheimer dementia, not the underlying disease, and the trial did not test whether the drug changes the course of the illness.
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This trial tested an antibody targeting tau tangles rather than amyloid plaques, in people with mild-to-moderate Alzheimer's. It slowed decline on one cognitive test by 42% compared with placebo, the first time an anti-tau antibody showed any cognitive benefit, but it did not help with daily-function scores, overall dementia staging (CDR-SB), or the MMSE, and it did not reduce tangle buildup seen on tau brain scans.
Why it matters
This trial tested an antibody targeting tau tangles rather than amyloid plaques, in people with mild-to-moderate Alzheimer's, and it slowed decline on one cognitive test by 42% compared with placebo, the first time an anti-tau antibody showed any cognitive benefit. However, it did not help with daily-function scores, overall dementia staging (CDR-SB), or the MMSE, and it did not reduce tangle buildup seen on tau brain scans.
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Alzheimer disease (AD) is the most common contributor to dementia in the world, but strategies that slow or prevent its clinical progression have largely remained elusive, until recently.
Why it matters
This review describes recent advances in biomarkers that can stage Alzheimer disease pathology and discusses evidence that certain anti-amyloid antibodies may slow cognitive decline in the mildly symptomatic phase. It also highlights newly identified therapeutic targets that might modify disease progression.
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Alzheimer's disease (AD) is the most common cause of dementia worldwide, but the molecular and cellular mechanisms underlying cognitive impairment remain poorly understood.
Why it matters
In prefrontal cortex tissue donated after death by 427 people (2.3 million cells), certain somatostatin inhibitory neurons were depleted in Alzheimer's disease. Two groups of inhibitory neurons were more abundant in people who kept high cognitive function late in life. The study also found increases in the cohesin complex and DNA damage response factors in excitatory neurons and oligodendrocytes. These are associations measured once, after death: they do not show that these cells protect memory or that any treatment would help.
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The incidence of Alzheimer's disease (AD), the leading cause of dementia, increases rapidly with age, but why age constitutes the main risk factor is still poorly understood.
Why it matters
In mouse models of Alzheimer's disease, damaged myelin — the insulating sheath around nerve fibres — led to more build-up of amyloid, the protein that forms plaques. The study reports that the machinery that produces amyloid accumulated in swollen nerve fibres, and that immune cells which normally surround plaques appeared to be drawn away to the nearby myelin damage instead. This is animal research into why ageing might raise risk; it tested no treatment and says nothing yet about people.
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The temporal evolutions and relative orderings of Alzheimer disease biomarkers, including CSF amyloid-β42 (Aβ42), Aβ40, total tau (Tau) and phosphorylated tau181 (pTau181), standardized uptake value ratio (SUVR) from the molecular imaging of cerebral fibrillar amyloid-β with PET using the 11C-Pittsburgh Compound-B (PiB), MRI-based hippocampal volume and cortical thickness and cognition have been hypothesized but not yet fully tested with longitudinal data for all major biomarker modalities among cognitively normal individuals across the adult lifespan starting from 18 years.
Why it matters
This large longitudinal study estimated the trajectories and ordering of Alzheimer's disease biomarkers across the adult lifespan in cognitively normal individuals. It describes how biomarkers change over time, not how to treat, cure, or prevent Alzheimer's disease.
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In DIAD, solanezumab was not associated with ARIA.
Why it matters
In the DIAN-TU-001 trial of gantenerumab or solanezumab in dominantly inherited Alzheimer disease, no ARIA-E was reported with solanezumab while gantenerumab was associated with ARIA-E compared with placebo, and most ARIA-E cases occurred at doses above 675 mg. Most ARIA-E resolved after dose adjustment and developing ARIA-E did not significantly increase the odds of trial discontinuation, so this study concerns the safety of these antibodies rather than showing a treatment or cure.
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We found that longitudinal changes in cognitive function measured by the cognitive composite decreased at low and high values of total sleep time (P < 0.001), time in non-REM (P < 0.001) and REM sleep (P < 0.001), sleep efficiency (P < 0.01) and <1 Hz and 1-4.5 Hz non-REM slow wave activity (P < 0.001) even after adjusting for age, CSF total tau/amyloid-β42 ratio, APOE ε4 carrier status, years of education and sex.
Why it matters
This study found that longitudinal cognitive function decreased at both low and high values of total sleep time, non-REM and REM sleep time, sleep efficiency, and non-REM slow wave activity, while cognitive function was stable within a middle range of these measures. It suggests certain levels of sleep may be important for maintaining cognitive function, but it does not show that changing sleep treats, cures, or prevents Alzheimer's disease.
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Although the performance of the different methods still has room for improvement, the results are promising and this methodology has a great potential as a support tool for clinicians and healthcare professionals.
Why it matters
This systematic review examined machine learning methods applied to neuroimaging data to predict whether people with mild cognitive impairment would develop Alzheimer's disease dementia. It reports that results are promising as a support tool for clinicians, but it is about prediction, not treating or curing the disease.
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65/100
In this Seminar, we highlight the main developments in the field of Alzheimer's disease.
Why it matters
This 2021 Lancet overview (a review, not a new study) reports that dementia prevalence is projected to double in Europe and triple worldwide by 2050, that Alzheimer's risk is 60–80% heritable with APOE the strongest of more than 40 genetic risk loci, and that PET scans and blood tests for amyloid β and phosphorylated tau "show great promise". It says multidomain lifestyle trials "suggest cognitive benefits" in people at increased risk of dementia, but also that lifestyle factors "do not directly affect Alzheimer's disease pathology". Anti-amyloid, anti-tau and anti-inflammatory drugs were in advanced trials when it was written.
From across this topic
10 of the 5,374 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.
- Use of florbetapir-PET for imaging beta-amyloid pathology
- Longitudinal plasma phosphorylated tau 181 tracks disease progression in Alzheimer's disease
- Biomarkers of neurodegeneration and glial activation validated in Alzheimer's disease assessed in longitudinal cerebrospinal fluid samples of Parkinson's disease
- Elevated plasma p-tau181 levels unrelated to Alzheimer's disease pathology in amyotrophic lateral sclerosis
- Reduced levels of amyloid beta-peptide antibody in Alzheimer disease
- Challenges in Managing Cerebral Amyloid Angiopathy in Alzheimer's Disease: Insights from a Case of Down Syndrome‐associated Alzheimer Disease (DSAD)
- Use of angiotensin receptor blockers and risk of dementia in a predominantly male population: prospective cohort analysis
- Alzheimer's Disease and Related Disorders Prevalence Differs by Appalachian Residence in Ohio
- Associations of Fully Automated CSF and Novel Plasma Biomarkers With Alzheimer Disease Neuropathology at Autopsy
- A high plasma concentration of TNF-alpha is associated with dementia in centenarians