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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Alzheimer's disease (AD) neuropathology is extremely heterogeneous, and the evolution from preclinical to mild cognitive impairment until dementia is driven by interacting genetic/biological mechanisms not fully captured by current clinical/research criteria.
Why it matters
In 113 participants, five distinct clusters were found based on cerebrospinal fluid biomarkers, and these clusters did not match the participants' clinical groups. Two clusters showed patterns of neurodegeneration not linked to classical Alzheimer's pathophysiology, and one was characterized by the neuroinflammation biomarker YKL-40. This biomarker-guided grouping may help identify patient subgroups, but it does not yet show any treatment, cure, or prevention effect.
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Extracellular deposition of amyloid β-protein (Aβ) in amyloid plaques and intracellular accumulation of abnormally phosphorylated τ-protein (p-τ) in neurofibrillary tangles (NFTs) represent pathological hallmark lesions of Alzheimer's disease (AD).
Why it matters
Using crossed transgenic mouse models, this study examined whether amyloid β accelerates the spread of tau pathology and how prion protein may be involved. It is animal research and does not show a treatment, cure, or prevention for people.
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We found that pharmacological activation of PPARA by the PPARA agonists gemfibrozil and Wy14643 induces autophagy in human microglia (HM) cells and U251 human glioma cells stably expressing the human APP (amyloid beta precursor protein) mutant (APP-p.M671L) and this effect is PPARA-dependent.
Why it matters
In human microglia and glioma cells, activating PPARA with gemfibrozil and Wy14643 induced autophagy, which the authors suggest may help clear amyloid beta. This is laboratory cell work, and the authors only suggest gemfibrozil be assessed as a possible treatment, so no benefit in patients is shown.
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Disease-modifying treatment trials are increasingly advanced to the prodromal or preclinical phase of Alzheimer's disease (AD), and inclusion criteria are based on biomarkers rather than clinical symptoms.
Why it matters
This study investigated which cerebrospinal fluid, MRI, amyloid and FDG-PET markers are associated with short-term cognitive decline and conversion from mild cognitive impairment to Alzheimer's disease dementia. It concerns prediction of conversion, not treatment, cure or prevention.
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Axonal degeneration, synaptic dysfunction, astroglial activation, and altered tau metabolism are involved already in preclinical AD.
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Between 2000 and 2017, deaths resulting from stroke, heart disease, and prostate cancer decreased, whereas reported deaths from AD increased 145%.
Why it matters
This 2019 report estimates that 5.8 million Americans have Alzheimer's dementia and that more than 16 million unpaid caregivers provided an estimated 18.5 billion hours of care in 2018. Its special report looks at brief cognitive assessments in primary care, finding only 16 percent of seniors receive them regularly.
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The vast increase in Alzheimer disease (AD) worldwide has grave implications for individuals, family support systems and the health-care systems that will attempt to cope with the disease.
Why it matters
This review examines whether problems with smell, hearing and vision could serve as early signs of Alzheimer's disease, noting that smell impairment is associated with prodromal Alzheimer's. The authors say more research is needed on how well these measures detect early disease, and no treatment or prevention is reported.
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Plasma neurofilament light (NFL) has been proposed as a blood-based biomarker for neurodegeneration in Alzheimer's disease (AD) and parkinsonian disorders.
Why it matters
Plasma neurofilament light was higher in people with Alzheimer's disease than in controls and other groups, and high levels correlated with poor cognition in Alzheimer's and Parkinson's disease. This supports its use as a biomarker of cognitive decline, not as a treatment, cure, or prevention.
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Mid-life obesity is an established risk factor for Alzheimer's disease (AD) dementia, whereas late-life obesity has been proposed as a protective state.
Why it matters
This study assessed the impact of late-life obesity on brain structure in 162 elderly controls from the Alzheimer's Disease Neuroimaging Initiative, taking into account weight loss as a potential confounder. The authors aimed to see if the proposed protective effect of late-life obesity on Alzheimer's disease risk could be explained by weight loss before cognitive decline.
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50/100
Amyloid pathology is associated with changes in structural MRI measures in CN and MCI.
Why it matters
This study found that amyloid pathology was linked to lower subcortical volumes and thinner cortex in Alzheimer's-signature regions in people with normal cognition and mild cognitive impairment. It suggests these MRI measures could be used to pre-screen subjects for anti-amyloid therapies in trials, but it does not itself test any treatment, cure, or prevention.
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ABSTRACTObjectives:Behavioral and psychological symptoms of dementia (BPSD) are nearly universal in dementia, a condition occurring in more than 40 million people worldwide.
Why it matters
An international expert panel reached consensus that behavioral and psychological symptoms in Alzheimer's disease should first be managed by identifying underlying causes and using caregiver training, environmental adaptations, person-centered care, and tailored activities. If medication is needed, citalopram and analgesia were prioritized ahead of antipsychotics for overall symptoms and agitation, while risperidone was prioritized for psychosis.
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Alzheimer's disease is the most prevalent cause of dementia, which is defined by the combined presence of amyloid and tau, but researchers are gradually moving away from the simple assumption of linear causality proposed by the original amyloid hypothesis.
Why it matters
This review discusses how aging and Alzheimer's disease are interwoven at molecular, cellular, and system levels, and notes that researchers are moving away from the simple idea that amyloid alone causes the disease. It is a summary of evidence and ideas, not a report of a treatment or cure.
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Between 2000 and 2015, deaths resulting from stroke, heart disease, and prostate cancer decreased, whereas deaths from AD increased 123%.
Why it matters
This 2018 report estimates that 5.7 million Americans have Alzheimer's dementia and that deaths from Alzheimer's increased 123% between 2000 and 2015. Its special report looks at the benefits of diagnosing Alzheimer's earlier, at the stage of mild cognitive impairment.
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Early identification of younger, non-demented adults at elevated risk for Alzheimer's disease (AD) is crucial because the pathological process begins decades before dementia onset.
Why it matters
In this sample of men in their 50s, a genetic risk score was linked to higher odds of having a mild memory problem, and diabetes was linked to a non-memory type of mild impairment. This is an early finding from one group of men and does not show that the score can prevent or treat Alzheimer's disease.
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Alzheimer's disease (AD) is the most common cause of progressive dementia in the elderly.
Why it matters
This review states that the metabolism of amyloid-beta and tau is influenced by autophagy, a lysosome-dependent process, and discusses therapeutic implications. It reports no treatment, cure or prevention that has been established.
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Differential diagnosis between dementia with Lewy bodies (DLB) and Alzheimer's disease (AD) is not straightforward, especially in the early stages of disease.
Why it matters
This retrospective study of 1221 cerebrospinal fluid samples compared Alzheimer biomarkers in patients with dementia with Lewy bodies and Alzheimer's disease, focusing on the prodromal stage. It is a diagnostic study and does not test any treatment, cure or prevention.
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The Study of Knowledge and Reactions to Amyloid Testing, a substudy of an AD prevention trial, involved 2 semistructured telephone interviews with 80 participants recruited from 9 study sites: 50 received elevated and 30 received not elevated amyloid PET scan results.
Why it matters
In telephone interviews with 50 cognitively normal adults aged 65–85 in an Alzheimer's prevention trial who were told their amyloid PET scan was "elevated", some wanted more than a yes/no label: they asked "how elevated their amyloid was, how close to the study threshold they were," or for "percentages, numbers, or a scale." The group was 98% white and 60% postgraduate-educated, so the results may not carry over to other people. The study looked at how people understand a scan result; it did not test any treatment.
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Gait is emerging as a potential diagnostic tool for cognitive decline.
Why it matters
This pilot study found that wearing body-worn sensors to measure gait in the clinic and at home was acceptable and feasible in people with early onset Alzheimer's disease. It supports further research on gait as a biomarker and does not report any treatment, cure, or prevention.
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Oxidative stress is implicated in the pathogenesis and progression of Alzheimer's disease (AD) and its earlier stage, amnestic mild cognitive impairment (aMCI).
Why it matters
This invited review pulls together a single laboratory's work linking amyloid-β (Aβ1-42) oligomers to oxidative damage in the brains of people with Alzheimer's, its earlier stage amnestic MCI, and Down syndrome with AD. It groups the downstream damage into four interrelated pathways it calls the "Quadrilateral of Neuronal Death": glucose metabolism, mTOR activation, the proteostasis network and protein phosphorylation. It notes that some of these changes appear even in preclinical AD. The authors' suggestion that drugs or lifestyle changes aimed at these pathways might slow progression is stated as their opinion, not a tested result.
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Immune mechanisms may be important in the pathogenesis of Alzheimer's disease (AD).
Why it matters
This study analyzed cerebrospinal fluid immune markers in healthy aging adults and in people without dementia, using tau and amyloid biomarkers to stage disease. It is an observational study and does not test any treatment that targets immune mechanisms.
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Levels of lithocholic acid were significantly enhanced in plasma of AD patients (50 ± 6 nM, p = 0.004) compared to healthy controls (32 ± 3 nM).
Why it matters
This study measured 20 bile acids in plasma and found lithocholic acid was significantly higher in Alzheimer's patients than in healthy controls, while levels in mild cognitive impairment were not significantly different from either group. The authors conclude four bile acids may be useful for diagnosing Alzheimer's from plasma despite limitations in diagnostic accuracy, but this is not a treatment.
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We hypothesized that cerebrospinal fluid (CSF) biomarkers of amyloid, neurodegeneration, and endothelial dysfunction would differ between older African Americans and Caucasians with normal cognition and cognitive impairment associated with AD.
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Metabolic dysfunction is a well-established feature of Alzheimer's disease (AD), evidenced by brain glucose hypometabolism that can be observed potentially decades prior to the development of AD symptoms.
Why it matters
This review describes how insulin resistance and metabolic disease may increase risk of Alzheimer's disease, possibly through mitochondrial dysfunction. It discusses possible mechanisms and imaging tools but does not show that treating insulin resistance prevents or cures Alzheimer's disease.
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CMBs are a common vascular pathology in the elderly.
Why it matters
Among 1677 nondemented participants, this study examined how brain volumes, infarcts and apolipoprotein E relate to deep versus lobar cerebral microbleeds, which are thought to reflect different underlying vessel diseases. These findings concern the interpretation of a brain imaging marker and do not provide a treatment, cure or prevention for Alzheimer's disease.
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Amyloid-beta (Aβ) plays a key role in the pathogenesis of Alzheimer's disease (AD), but little is known about the proteoforms present in AD brain.
Why it matters
Using mass spectrometry on brains of six people with confirmed Alzheimer's disease, this study found 26 unique amyloid-beta proteoforms, with truncated forms making up much of the total and segregating between soluble and insoluble aggregates. The authors state this heterogeneity deepens understanding of the disease and offers avenues for investigation, but it is laboratory work on a small number of brains and does not test 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.
- Neural biomarker diagnosis and prediction to mild cognitive impairment and Alzheimer's disease using EEG technology
- Comparison of tau spread in people with Down syndrome versus autosomal-dominant Alzheimer's disease: a cross-sectional study
- Alzheimer's trials: A cul-de-sac with no end in sight
- A genome-wide association meta-analysis of plasma Aβ peptides concentrations in the elderly
- Japanese and North American Alzheimer's Disease Neuroimaging Initiative studies: Harmonization for international trials
- Indirect Costs of Alzheimer's Disease: Unpaid Caregiver Burden and Patient Productivity Loss
- Eligibility for Anti-Amyloid Treatment in a Population-Based Study of Cognitive Aging
- Comparative Brain and Serum Exosome Expression of Biomarkers in an Experimental Model of Alzheimer-Type Neurodegeneration: Potential Relevance to Liquid Biopsy Diagnostics
- Alzheimer's disease as homeostatic responses to age-related myelin breakdown
- The Biological Intersection Between Chemotherapy-Related Cognitive Impairment and Alzheimer Disease