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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61/100
Alzheimer's disease is the most common cause of dementia.
Why it matters
This seminar reviews the epidemiology, genetics, pathogenesis, diagnosis, and treatment of Alzheimer's disease, noting that familial Alzheimer's disease is a very rare autosomal dominant early-onset disease caused by mutations in the amyloid precursor protein and presenilin genes. It states that the cause of the much more common sporadic form is unknown, probably because the disease is heterogeneous, caused by ageing in concert with a complex interaction of genetic and environmental risk factors.
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Cognitive function was inversely related to all measures of disease pathology, indicating lower function at more severe levels of pathology.
Why it matters
In 89 older people from the Rush Memory and Aging Project who were examined at autopsy, more Alzheimer's-type brain pathology went with lower thinking ability. That link was weaker in people with larger social networks: "even at more severe levels of global disease pathology, cognitive function remained higher" for them, a pattern also seen with tau tangles but not amyloid load, and unchanged after adjusting for activities, depressive symptoms and chronic diseases. The authors say this "suggest[s]" social networks modify how some pathology relates to cognition. It is an observational association and does not show that social networks prevent or change the disease.
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Diabetes and current smoking were the strongest risk factors, but clusters including hypertension and heart disease also increased the risk of AD.
Why it matters
In this cohort, diabetes, hypertension, heart disease, and current smoking were each linked to higher risk of Alzheimer disease, and risk rose with the number of these factors present. This identifies risk factors that might be targets for prevention but does not test a treatment.
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61/100
This observational study provides further evidence that lipid-lowering agents are associated with decreased risk of dementia, whereas hyperlipidemia is associated with increased odds for non-Alzheimer-disease-type dementia.
Why it matters
In this French population study, people taking cholesterol-lowering drugs were less likely to have dementia, while those with high cholesterol were more likely to have it. This kind of study can only show an association, not that these drugs prevent or treat Alzheimer's disease.
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We developed an anatomical mapping technique to detect hippocampal and ventricular changes in Alzheimer disease (AD).
Why it matters
Using serial MRI in 12 Alzheimer patients and 14 controls, hippocampal atrophy and ventricular expansion were faster in Alzheimer disease than in controls, and these changes were linked with cognitive decline. Temporal horn expansion maps were more sensitive to disease progression than maps of hippocampal atrophy.
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Plasma levels of inflammatory proteins are increased before clinical onset of dementia, Alzheimer disease, and vascular dementia.
Why it matters
In this case-cohort study, higher plasma levels of alpha1-antichymotrypsin, interleukin 6, and to a lesser extent C-reactive protein were associated with an increased risk of dementia. The study reports associations and does not show that reducing inflammation prevents dementia.
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The results of this study indicate that rofecoxib or low-dose naproxen does not slow cognitive decline in patients with mild-to-moderate AD.
Why it matters
In this one-year, double-blind trial at 40 Alzheimer's Disease Cooperative Study centers, 351 people with mild-to-moderate Alzheimer disease took rofecoxib, low-dose naproxen or a placebo. Average decline on the ADAS-Cog memory-and-thinking test was 7.6 points with rofecoxib, 5.8 with naproxen and 5.7 with placebo, which the authors report as not significantly different, and secondary measures "showed no consistent benefit of either treatment." The authors conclude these drugs do "not slow cognitive decline" in this group, and fatigue, dizziness, high blood pressure and serious side effects were more common on the active drugs.
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Amyloid-beta peptide (Abeta) has a key role in the pathogenesis of Alzheimer disease (AD).
Why it matters
This 2003 case report examined the brain of one person with Alzheimer's disease who had been immunized with amyloid-beta (AN-1792), and compared it with seven unimmunized Alzheimer's cases. The brain still showed the diagnostic features of Alzheimer's, but had "extensive areas of neocortex with very few Abeta plaques", which the authors say "strongly resemble" changes seen after immunotherapy in mice and "suggest" the immune response cleared plaques in this patient. It is a single patient, and the record reports no cognitive or clinical outcome, so it shows a change in brain tissue, not a benefit to the person.
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Alzheimer's disease is characterized by a slow, progressive decline in cognitive function and behaviour.
Why it matters
This double-blind, randomized, placebo-controlled trial tested Salvia officinalis extract in patients with mild to moderate Alzheimer's disease. It evaluates a possible herbal treatment, not a proven cure or prevention for the disease.
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Carriers of the apolipoprotein E (APOE) epsilon4 allele show significantly higher risk of Alzheimer disease (AD).
Why it matters
This study found a statistical interaction between APOE genotype and gender, with women carrying an APOE epsilon4 allele having a substantially greater risk of Alzheimer's disease than men carrying the allele. This is about risk patterns and does not provide a treatment, cure, or prevention.
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Age, sex, functional limitation, and malnutrition seem to be the strongest predictors of death for patients with Alzheimer's disease in nursing homes.
Why it matters
Among nursing home residents with Alzheimer's disease, older age, male sex, physical limitations, malnutrition, pressure ulcers, diabetes and cardiovascular disease were linked to higher mortality. This describes factors associated with death and does not test a treatment, cure or prevention.
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APOE genotyping does not provide sufficient sensitivity or specificity to be used alone as a diagnostic test for Alzheimer's disease, but when used in combination with clinical criteria, it improves the specificity of the diagnosis.
Why it matters
Adding APOE genotype information to a clinical diagnosis did not clearly improve the accuracy of diagnosing Alzheimer's disease in this study. The clinical diagnosis alone had high sensitivity but low specificity, and the APOE epsilon4 allele by itself was not accurate enough to confirm or rule out the disease.
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61/100
Tacrine stabilizes or improves specific behavioral deficits and symptoms in AD.
Why it matters
In this exploratory analysis of a 30-week trial, a greater percentage of patients on tacrine improved or stabilized on 8 of 11 ADAS-cognitive items compared with placebo. It reports effects on language, praxis, and noncognitive problems in Alzheimer's disease but does not show a cure or prevention.
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In patients with moderately severe impairment from Alzheimer's disease, treatment with selegiline or alpha-tocopherol slows the progression of disease.
Why it matters
In a two-year trial of 341 patients with moderately severe Alzheimer's disease, selegiline, vitamin E (alpha-tocopherol) or both were compared with placebo. Unadjusted results showed no significant difference, but after adjusting for differences in starting Mini-Mental State Examination scores, all three treatments delayed outcomes such as death, institutionalization or severe dementia.
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Why it matters
Sets out the amyloid cascade hypothesis as an account of how Alzheimer's disease comes about. It is a proposed explanation that shapes where treatments are looked for, not a treatment or a test of one.
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61/100
We studied the accumulation of neurofibrillary tangles (NFTs) and senile plaques (SPs) in 10 Alzheimer's disease patients who had been examined during life.
Why it matters
This study of 10 Alzheimer's disease patients found that the severity of dementia was positively related to the number of neurofibrillary tangles in the neocortex, but not to the degree of senile plaque deposition. It suggests neurofibrillary tangles parallel the duration and severity of Alzheimer's disease.
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The Neuropathology Task Force of the Consortium to Establish a Registry for Alzheimer's Disease (CERAD) has developed a practical and standardized neuropathology protocol for the postmortem assessment of dementia and control subjects.
Why it matters
The CERAD Neuropathology Task Force developed a standardized postmortem protocol providing definitions such as definite, probable, and possible Alzheimer's disease to indicate levels of diagnostic certainty and assure common language. In pretesting, 84% of dementia cases clinically diagnosed as probable Alzheimer's disease met CERAD neuropathologic criteria for definite Alzheimer's disease.
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Clinical and neuropathologic evidence points to the development of Alzheimer's disease (AD) in seven Down's syndrome patients above age 40.
Why it matters
In seven adults with Down syndrome over age 40, followed for 2.5 to 9.2 years, dementia began with loss of visual memory, then problems with learning and daily and social functioning, and ended with seizures and urinary incontinence. After death, every brain had many Alzheimer's plaques and tangles; four also showed small strokes and five showed amyloid deposits in blood-vessel walls. The authors conclude that repeated testing over time, plus lab tests that rule out other causes, can diagnose Alzheimer's even in people with severe or profound intellectual disability. This was a series of seven cases with no comparison group, and it did not test any treatment.
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Over a mean follow-up of 8.4 years (range, Conclusions and relevance This cohort study of older adults found that adherence to a dietary pattern with lower inflammatory potential was associated with lower dementia risk among individuals with AD pathology and broader neurobiological risk.
Why it matters
This cohort study found that a dietary pattern with lower inflammatory potential was associated with lower dementia risk among older adults with Alzheimer's pathology and broader neurobiological risk. The findings support targeted dietary prevention strategies, but the study was observational.
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This study directly compared four different commercial/lab p-tau217 blood tests (Lumipulse, ALZpath, Johnson & Johnson, and NULISA) in 344 people from two community cohorts, most of whom were cognitively normal or had only mild changes.
Why it matters
Four different p-tau217 blood tests were similarly good at detecting amyloid buildup (AUC 0.84-0.90) but all performed poorly at detecting tau tangles (AUC 0.52-0.61) in mostly cognitively normal people. This suggests these blood tests are better suited to flagging amyloid than tau pathology at this early stage, and it is a diagnostic comparison, not a treatment finding.
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Blood biomarkers have emerged as accurate tools for detecting Alzheimer's disease (AD) pathology, offering a minimally invasive alternative to traditional diagnostic methods such as imaging and cerebrospinal fluid (CSF) analysis.
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The aim of this study was to evaluate longitudinal associations of multimodal core 1 AD biomarkers with cognition in a cognitively unimpaired (CU) population at increased risk of AD dementia.
Why it matters
This study tracked how multiple Alzheimer's biomarkers relate to cognition over time in cognitively unimpaired people at increased risk. It is observational and does not test whether any treatment changes this relationship.
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Plasma p-tau217 is an accurate indicator of amyloid pathology in a heterogeneous cohort and is superior to other plasma biomarkers assessed.
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EOAD, although sharing genes with LOAD, harbors unique genes and pathways that could be used to create better prediction models or target identification.
Why it matters
This genetic study found eight new gene regions linked to early-onset Alzheimer's disease, involving microglia activation, glutamate production, and signaling pathways. These findings could help build better prediction models or identify new treatment targets, though they are genetic associations rather than proven treatments.
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Our findings suggest that poor olfaction is associated with multiple AD-related and other neurodegenerative processes.
Why it matters
In 1,545 older adults, poorer sense of smell was linked to higher levels of several Alzheimer's-related and neurodegeneration blood markers. This cross-sectional study shows an association only and cannot show whether smell loss causes or predicts disease.
From across this topic
9 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 9. The same 9 appear here every time.
- Strong diagnostic performance of plasma ptau217 for CSF biomarker-defined young-onset Alzheimer disease in a diagnostically heterogeneous clinical cohort
- Personalized whole-brain neural mass models reveal combined Aβ and tau hyperexcitable influences in Alzheimer's disease
- Vitamin B(12) and folate in relation to the development of Alzheimer's disease
- Perivascular space and white matter hyperintensities in Alzheimer's disease: associations with disease progression and cognitive function
- Genetics of Alzheimer's disease in Caribbean Hispanic and African American populations
- The lower hippocampus global connectivity, the higher its local metabolism in Alzheimer disease
- Self-rated and informant-rated everyday function in comparison to objective markers of Alzheimer's disease
- Investigating the Impact of NMDA Receptor Organization and Biological Sex in the APPswe/PS1dE9 Mouse Model of Alzheimer’s Disease
- Presymptomatic cortical thinning in familial Alzheimer disease: A longitudinal MRI study