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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In this trial, memantine did not show an advantage over placebo based on protocol-specified primary or secondary analyses in patients with mild to moderate AD on stable ChEI regimens.
Why it matters
In a 24-week randomized trial of 433 people with mild to moderate Alzheimer's (MMSE 10–22) who were already on a stable cholinesterase inhibitor (donepezil, rivastigmine or galantamine), adding memantine 20 mg once daily showed "no statistically significant differences" from placebo on thinking (ADAS-cog), clinician-rated change (CIBIC-Plus), daily activities, behaviour or MMSE. Side-effect rates were similar in both groups. The result applies to this add-on setting and time frame. It does not test memantine alone or in more advanced disease.
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The objective of this study was to determine whether treatment with the nonselective nonsteroidal anti-inflammatory drug (NSAID) indomethacin slows cognitive decline in patients with Alzheimer's disease (AD).
Why it matters
This randomised controlled trial found that one year of treatment with the anti-inflammatory drug indomethacin did not slow cognitive decline in people with mild to moderate Alzheimer's disease. It reports a null result for this treatment.
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66/100
Alzheimer disease (AD) has a significant impact on caregivers.
Why it matters
In this substudy of the IDEAL trial, more than 70% of 1059 caregivers preferred rivastigmine patches over capsules for ease of use and satisfaction. It addresses caregiver preference for a delivery method and does not show that the drug treats, cures, or prevents Alzheimer's disease.
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Pittsburgh Compound B PET findings match histopathologic reports of beta-amyloid (Abeta) distribution in aging and dementia.
Why it matters
Using PET imaging, this study found that amyloid burden was elevated in every person with Alzheimer's disease, lower and more variable in dementia with Lewy bodies, absent in frontotemporal dementia, and present in some people with mild cognitive impairment and even some healthy controls. It shows that amyloid imaging can reveal brain changes, but it does not provide a treatment, cure or prevention.
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Patients treated with LY451395 did not show a statistically significant separation from patients taking placebo on the Alzheimer's Disease Assessment Scale-Cognitive Subscale, the primary outcome measure.
Why it matters
In 181 patients with mild to moderate Alzheimer's disease, LY451395 did not show a statistically significant separation from placebo on the primary cognitive outcome, with only a marginal change on the Neuropsychiatric Inventory. This drug did not demonstrate a cognitive benefit.
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Alzheimer's disease is a common and devastating disease for which there is no readily available biomarker to aid diagnosis or to monitor disease progression.
Why it matters
This case-control study found that certain plasma proteins, including complement factor H and alpha-2-macroglobulin, were elevated in people with Alzheimer's disease and correlated with disease severity. These findings suggest blood may be a source of biomarkers, but they do not provide a treatment, cure, or prevention.
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66/100
Diabetes mellitus did not increase the risk of incident AD in the Framingham cohort overall; however, DM may be a risk factor for AD in the absence of other known major AD risk factors.
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Longitudinal studies will be required to determine the association of elevated [(11)C]PIB binding and risk of developing dementia of the Alzheimer type.
Why it matters
In 41 people without dementia (aged 20 to 86) and 10 people with Alzheimer-type dementia, each given one PET scan with the amyloid tracer PIB, the authors report that elevated tracer binding in nondemented people "suggests that [(11)C]PIB amyloid imaging may be sensitive for detection of a preclinical Alzheimer disease state." Because each person was scanned once, the study could not show whether that binding leads to dementia; the authors write that "longitudinal studies will be required" to test that. It is an imaging study and does not test any treatment or prevention.
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Atorvastatin treatment may be of some clinical benefit and could be established as an effective therapy for Alzheimer disease if the current findings are substantiated by a much larger multicenter trial.
Why it matters
In this small pilot trial, atorvastatin reduced circulating cholesterol levels and produced a positive signal on each clinical outcome measure compared with placebo, reaching significance for one measure. Because it was a preliminary proof-of-concept study, the results are not definitive.
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This cost-consequence analysis reveals economic benefits of treatment of moderate to severe AD with donepezil.
Why it matters
In 290 patients with moderate to severe Alzheimer's disease, donepezil was associated with a net societal cost saving of Can 332 dollars over 24 weeks compared with placebo. This is an economic evaluation of costs, not evidence about treating, curing, or preventing Alzheimer's disease.
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Patients with Alzheimer disease (AD) commonly exhibit psychosis and behavioral disturbances that impair patient functioning, create caregiver distress, and lead to institutionalization.
Why it matters
In this 6-week trial of 206 nursing home residents with Alzheimer disease and psychotic or behavioral symptoms, low-dose olanzapine (5 and 10 mg/d) produced significant improvement in agitation/aggression and psychosis compared with placebo. Low-dose olanzapine was significantly superior to placebo and well tolerated in this population.
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This multicentre, open-label study evaluated the long-term efficacy and safety of donepezil in the treatment of patients with mild to moderately severe Alzheimer's disease (AD).
Why it matters
This open-label study followed 133 patients with mild to moderately severe Alzheimer's disease who took donepezil for up to 240 weeks to assess long-term efficacy and safety. It reports on an existing drug's long-term use, not on curing or preventing the disease.
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66/100
Our data from a population-based study support the hypothesis that estrogen-replacement therapy is associated with a reduced prevalence of Alzheimer's disease in postmenopausal women.
Why it matters
In this survey of postmenopausal women in Italy, estrogen use was less frequent among Alzheimer's disease patients than among nonpatients, and the inverse association remained significant after adjustment for several factors. This is an observed association in a population survey, not evidence that estrogen-replacement therapy prevents or treats Alzheimer's disease.
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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.
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.
- A Novel Mouse Model for Investigating ARIAs in Response to Anti-Abeta Immunotherapy
- Cognitive reserve and clinical progression in Alzheimer disease: A paradoxical relationship
- The role of microbial amyloid in neurodegeneration
- Cognitive and functional neuroimaging correlate for anosognosia in mild cognitive impairment and Alzheimer's disease
- Test-retest reliability of memory task functional magnetic resonance imaging in Alzheimer disease clinical trials
- Arthritis and anti-inflammatory agents as possible protective factors for Alzheimer's disease: a review of 17 epidemiologic studies
- Plasma proteomics for the identification of Alzheimer disease
- Traumatic brain injury history is associated with an earlier age of dementia onset in autopsy-confirmed Alzheimer's disease
- Association between CSF biomarkers and incipient Alzheimer's disease in patients with mild cognitive impairment: a follow-up study
- Reduced retinal thickness and risk of Alzheimer’s disease: a bidirectional two-sample Mendelian randomization study