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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The search for biomarkers as a diagnostic aid to the identification of patients in pre-dementia stages is a fast growing research area.
Why it matters
This systematic review and meta-analysis of 16 studies found that in people diagnosed with mild cognitive impairment, low cerebrospinal fluid amyloid-beta 42 along with high total tau and high phosphorylated tau helped predict conversion to Alzheimer's compared with controls. These biomarkers may add precision to diagnosis, but the study tests no treatment or cure.
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61/100
Why it matters
Uses plasma signaling proteins to classify and predict clinical Alzheimer's diagnosis.
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Prior work has suggested that obesity and overweight as measured by body mass index (BMI) increases risk of dementia.
Why it matters
In this large cohort, being obese at midlife was linked to a higher risk of Alzheimer's disease and an even higher risk of vascular dementia about 36 years later. This identifies midlife obesity as a risk factor but does not test a treatment or cure.
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Although memory complaints are associated with an increased risk of Alzheimer's disease in persons with cognitive impairment as well as in persons with normal cognition, they are commonly considered of less importance than objective cognitive measures.
Why it matters
This study examined whether the link between subjective memory complaints and Alzheimer's disease risk varies with a person's education. It is about interpreting memory complaints as a risk signal, not about treating, curing or preventing the disease.
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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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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.
From across this topic
9 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 9. The same 9 appear here every time.
- Neuroinflammation - an early event in both the history and pathogenesis of Alzheimer's disease
- Concordance between brain 18F-FDG PET and cerebrospinal fluid biomarkers in diagnosing Alzheimer's disease
- Amyloid Deposition Is Associated with Impaired Default Network Function in Older Persons without Dementia
- Functional Specificity of Astrocyte Subtypes in Alzheimer’s Disease: Decoding Disease Mechanisms Through Network-based Analysis of Integrated Single-Nuclei Multi-Omic Data
- Proteolytic therapeutic modalities for amyloidoses: Insights into immunotherapy, PROTAC, and photo-oxygenation
- Strong diagnostic performance of plasma ptau217 for CSF biomarker-defined young-onset Alzheimer disease in a diagnostically heterogeneous clinical cohort
- 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