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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Age-associated changes in brain imaging and fluid biomarkers are characterized and compared in presenilin 1 (PSEN1)E280A mutation carriers and noncarriers from the world's largest known autosomal dominant Alzheimer disease (AD) kindred.
Why it matters
In this cross-sectional study of 54 members of a single family with the PSEN1 E280A mutation, researchers compared age-related changes in brain imaging and fluid biomarkers between mutation carriers and noncarriers. Because the study only measured biomarkers at one point in time, it cannot show whether these markers predict or cause later cognitive decline.
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High adherence to all three diets may reduce AD risk.
Why it matters
In 923 people aged 58 to 98 followed for an average of 4.5 years, closer adherence to the MIND diet, a hybrid of the Mediterranean and DASH diets, was associated with lower rates of Alzheimer's disease. High adherence to the Mediterranean and DASH diets was also associated with lower rates, and the authors say even moderate adherence to the MIND diet may decrease risk.
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Use of selective in-vivo tau imaging will enable improved understanding of tau aggregation in the brain, facilitating research into causes, diagnosis, and treatment of major tauopathies such as Alzheimer's disease, progressive supranuclear palsy, corticobasal syndrome, chronic traumatic encephalopathy, and some variants of frontotemporal lobar degeneration.
Why it matters
This 2015 review looks ahead to brain scans that can show the protein tau in living people, across Alzheimer's disease and other "tauopathies" such as progressive supranuclear palsy, corticobasal syndrome, chronic traumatic encephalopathy and some forms of frontotemporal lobar degeneration. Post-mortem studies had linked tau deposits to poorer thinking and to brain degeneration, and the authors argue that tau imaging would let researchers track where and how fast tau builds up over time. They say that only "once validated" might it become a test for diagnosis, prognosis or disease progression, or a tool for anti-tau drug trials; the review itself reports no new patient data and tests no treatment.
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Recent epidemiological and clinico-pathological data indicate considerable overlap between cerebrovascular disease (CVD) and Alzheimer's disease (AD) and suggest additive or synergistic effects of both pathologies on cognitive decline.
Why it matters
This review of brain-pathology evidence reports that "up to 84%" of older people examined show blood-vessel damage alongside Alzheimer's changes, most often cerebral amyloid angiopathy and small vessel disease; the record does not say which group of brains that upper figure comes from. It describes small strokes as having no added effect on decline once Alzheimer's is advanced, because they are "overwhelmed by the severity of Alzheimer pathology", while in early stages vascular lesions "may" lower the threshold for dementia. This is a summary of existing findings that "suggest" the two kinds of damage add up; it is not a trial and does not show that treating vascular disease prevents Alzheimer's.
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This cluster analysis of cortical thickness of the entire brain showed that AD dementia in the earlier stages can be categorized into various anatomical subtypes, with distinct clinical features.
Why it matters
Among 152 patients with early Alzheimer disease dementia, MRI cortical thickness measurements revealed three distinct patterns of atrophy. This shows that Alzheimer disease can look anatomically different across patients, but it does not test treating, curing, or preventing the disease.
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Microbleed presence was associated with lower CSF Aβ42 in AD and vascular dementia (standardized beta = -0.09, P = .003; standardized beta = -0.30, P = .01), and higher CSF tau in controls (standardized beta = 0.10, P = .03).
Why it matters
In this cross-sectional study, markers of cerebral small-vessel disease such as microbleeds and white matter hyperintensities were associated with lower spinal fluid amyloid beta in some groups, with effects mostly attributable to APOE epsilon4 carriers. This describes associations between vascular markers and Alzheimer's pathology, not treatment or prevention.
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Our data suggest that interactions between biomarkers in AD result in a 2-phase phenomenon of pathological cortical thickening associated with low CSF Aβ, followed by atrophy once CSF p-tau becomes abnormal.
Why it matters
In these normal controls, cortical atrophy occurred only in people with both abnormal CSF β-amyloid and abnormal CSF phospho-tau, and the relationship between each biomarker and cortical thickness depended on the other. This cross-sectional finding suggests these biomarkers interact in preclinical Alzheimer disease, but it cannot show cause or predict outcomes.
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We describe a 2-feature biomarker approach to classifying elderly CN subjects that is complementary to the National Institute on Aging-Alzheimer's Association preclinical staging criteria.
Why it matters
In cognitively normal older adults, the rate of amyloid accumulation was not affected by hippocampal neurodegeneration at baseline, while brain atrophy was greatest in those with both amyloid and neurodegeneration. This supports a model of how biomarkers evolve over time and does not test a treatment, cure, or prevention.
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This study was designed to evaluate whether subjects with amyloid beta (Aβ) pathology, detected using florbetapir positron emission tomorgraphy (PET), demonstrated greater cognitive decline than subjects without Aβ pathology.
Why it matters
This study used amyloid PET imaging to see whether people with amyloid pathology showed greater cognitive decline over 36 months than those without it, across cognitively normal, mild cognitive impairment, and Alzheimer's disease groups. It examines a marker for predicting decline, not a treatment, cure or prevention.
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From a total sample of 559 older adults from the Massachusetts Alzheimer's Disease Research Center longitudinal cohort, 454 were included in the primary analysis: 283 with clinically normal cognition (CN), 115 with mild cognitive impairment (MCI), and 56 with subjective cognitive concerns (SCC) but no objective impairment, a proposed transitional group between CN and MCI.
Why it matters
In this group of older adults, better memory-semantic scores predicted slower progression to a worse diagnosis, and affective factors also predicted faster progression. These findings point to possible markers for identifying who may decline sooner, but they do not show that treating these factors changes the course of Alzheimer's disease.
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Most experts consider that memantine has a symptomatic treatment, but clinical trials have not yet provided compelling evidence to support a disease-modifying effect.
Why it matters
In this small trial, people with moderate to severe Alzheimer disease treated with memantine showed less cognitive decline and less decline in brain glucose metabolism than those on placebo, but there were no significant effects on cerebrospinal fluid markers. The authors note that larger and longer studies are needed, and this does not establish a disease-modifying effect.
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Cross-sectional and longitudinal studies.
Why it matters
This study examined whether regional cortical thinning and CSF Alzheimer's biomarkers were associated with apathy and hallucinations across the Alzheimer's disease spectrum. It is an observational study of symptoms and brain measures, not a test of any treatment, cure, or prevention.
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The diagnostic guidelines of Alzheimer's disease (AD) have recently been updated to include brain imaging and cerebrospinal fluid (CSF) biomarkers, with the aim of increasing the certainty of whether a patient has an ongoing AD neuropathologic process or not.
Why it matters
This review says cerebrospinal fluid biomarkers have high diagnostic accuracy for Alzheimer's dementia and for predicting incipient Alzheimer's disease in people with mild cognitive impairment. It notes that blood biomarkers are harder to find and that encouraging results need verification in independent studies, so this is about diagnosis and prediction, not treatment or cure.
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Hexanucleotide repeat expansions in the chromosome 9 open reading frame 72 (C9orf72) gene underlie a significant fraction of frontotemporal dementia and amyotrophic lateral sclerosis.
Why it matters
This case-control study genotyped the C9orf72 repeat expansion in people with clinically diagnosed late-onset Alzheimer's disease and in control subjects. It examined frequency only and reports no treatment, cure or prevention.
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Hormonal changes associated with the menopausal transition and postmenopause have the potential to influence processes linked to Alzheimer's disease symptoms and pathogenesis, but effects of menopause on Alzheimer risk can be addressed only indirectly.
Why it matters
Across nine randomized trials, estrogen-containing hormone therapy did not improve cognitive symptoms in women who already had Alzheimer's disease. One trial found that combined estrogen plus progestogen started at age 65 or older increased dementia risk, while the idea that starting hormone therapy closer to menopause might reduce risk comes only from observational research and has not been tested in clinical trials.
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Apolipoprotein E (Apo-E) is a major cholesterol carrier that supports lipid transport and injury repair in the brain.
Why it matters
This 2013 review summarises what was then known about the APOE gene: compared with the common ε3 version, carriers of ε4 are at increased risk of Alzheimer's disease, and of amyloid build-up in brain blood vessels and age-related cognitive decline, while ε2 is linked to lower risk. It describes how the protein versions differ in handling amyloid-β, brain lipids, glucose metabolism, inflammation and mitochondrial function, and discusses how therapies targeting apolipoprotein E might be designed. It reports no new data, gives no risk figures, and tests no treatment, so it cannot tell any individual how likely they are to develop the disease.
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The Alzheimer's Disease Neuroimaging Initiative (ADNI) measures abilities broadly related to executive function (EF), including WAIS-R Digit Symbol Substitution, Digit Span Backwards, Trails A and B, Category Fluency, and Clock Drawing.
Why it matters
Researchers combined standard ADNI tests (including Trails A and B, Category Fluency and Clock Drawing) into one executive-function score, "ADNI-EF", using data from 800 ADNI participants. In 390 people with mild cognitive impairment who were followed over time, ADNI-EF "showed the greatest change over time, followed closely by Category Fluency". That makes it a measurement tool for research studies. It is not a treatment, and the stored record does not report how well it predicted dementia.
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Alzheimer disease (AD) is associated with aberrant processing of the amyloid precursor protein (APP) by γ-secretase, via an unknown mechanism.
Why it matters
This study found that mitochondria-associated ER membrane function and ER-mitochondrial communication are increased in cells with presenilin mutations and in fibroblasts from patients with familial and sporadic Alzheimer's disease. These were cell-based experiments, so it is not yet known whether targeting these membranes could treat or prevent Alzheimer's disease.
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This study provides data on whether tailored nutritional care is beneficial to home-dwelling AD patients and their spouses.
Why it matters
This is a study protocol describing a planned trial of individualized nutritional care for people with Alzheimer's disease living at home, so no results on treating or preventing the disease are available. The main outcome it plans to measure is weight change, not whether the disease itself is affected.
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56/100
This study will provide clinically relevant data on the likelihood and time to relapse, and predictors of relapse, in patients switched from risperidone to placebo after response to risperidone treatment.
Why it matters
This paper describes the design of a trial on discontinuing the antipsychotic risperidone in patients with Alzheimer disease who responded to it. It aims to provide data on relapse likelihood and timing, not on treating, curing, or preventing Alzheimer's disease itself.
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In vivo imaging and quantification of amyloid-β plaque (Aβ) burden in small-animal models of Alzheimer's disease (AD) is a valuable tool for translational research such as developing specific imaging markers and monitoring new therapy approaches.
Why it matters
This study in an APP/PS1 mouse model showed that [11C]PiB PET could detect amyloid-beta plaques in living mouse brains, validated against several laboratory methods. It is animal research on an imaging method, not a treatment, so it does not show how to cure or prevent Alzheimer's disease in people.
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Early detection of prodromal Alzheimer disease (AD) is important because new disease-modifying therapies are most likely to be effective when initiated during the early stages of disease.
Why it matters
This study took spinal-fluid samples from 137 people who already had mild cognitive impairment and followed them for a median of 9.2 years (range 4.1–11.8) to see who developed Alzheimer dementia. Its title reports that one amyloid marker (β-amyloid 1-42) was already fully changed 5 to 10 years before dementia began, while tau markers were not. The summary held here ends before the results, so no accuracy figures are available, and as an observational study it cannot show that amyloid causes dementia or that any treatment would prevent it.
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Neuropsychiatric symptoms (NPS) are core features of Alzheimer's disease and related dementias.
Why it matters
This review states that neuropsychiatric symptoms are core features of Alzheimer's disease and can appear very early, including in mild cognitive impairment, but that reliable treatments for these symptoms have not been found and widely used medications carry notable risks. It offers no treatment, cure or prevention for Alzheimer's disease itself.
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Apolipoprotein E (APOE) dependent lifetime risks (LTRs) for Alzheimer Disease (AD) are currently not accurately known and odds ratios alone are insufficient to assess these risks.
Why it matters
Combining APOE genotypes from 7,351 people with Alzheimer's and 10,132 without (all of Caucasian ancestry) with US population incidence data, this study estimated the chance of developing Alzheimer's by age 85 at 51% for men and 60% for women with two APOE4 copies, and 23–30% with one copy, compared with 11–14% for the population as a whole. Using French incidence data instead gave broadly similar figures, though higher for women with two copies (68%). The authors say these risks look more like a major disease gene such as BRCA1 than a minor genetic risk factor, but they are group estimates, not a prediction for any individual.
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The INNOTEST and INNO-BIA CSF platforms perform equally well in identifying individuals with underlying amyloid plaque pathology.
Why it matters
In 103 research volunteers, this study ran spinal-fluid amyloid and tau on two widely used lab platforms and checked both against amyloid PET brain scans. The platforms gave raw numbers that differed about 2- to 6-fold but ranked people similarly and "perform equally well" at spotting amyloid plaques, so each test needs its own cutoff, and the tau-to-amyloid ratios did better than any single marker. It compares diagnostic tests and does not test any treatment, cure, or prevention.
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.
- Enrichment through biomarkers in clinical trials of Alzheimer's drugs in patients with mild cognitive impairment
- Alpha-synuclein in Lewy body disease and Alzheimer's disease
- Melissa officinalis extract in the treatment of patients with mild to moderate Alzheimer's disease: a double blind, randomised, placebo controlled trial
- EEG SIGNAL ANALYSIS FOR CLASSIFYING ALZHEIMER’S AND FRONTOTEMPORAL DEMENTIA DISORDERS USING ENSEMBLE METHODS
- Abeta toxicity in Alzheimer's disease: globular oligomers (ADDLs) as new vaccine and drug targets
- MMSE–CDR‐SB residual as an exploratory indicator of deviation from an Alzheimer's disease–typical cognitive–functional pattern
- Alzheimer's CSF markers in older schizophrenia patients
- Targeting of nonlipidated, aggregated apoE with antibodies inhibits amyloid accumulation
- Fruit and vegetable juices and Alzheimer's disease: the Kame Project
- Morphologic association between microglia and senile plaque amyloid in Alzheimer's disease