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) is the leading cause of dementia.
Why it matters
This review describes the amyloid plaques and tau tangles of Alzheimer's disease and notes that most cases are late-onset with no clear cause. It discusses genetic and other risk contributors but reports no treatment or cure.
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Alzheimer disease is more than a pure proteopathy.
Why it matters
This 2018 review summarises earlier research and adds no new data. It describes APOE, which it calls "the strongest genetic risk factor for Alzheimer disease", as acting on the disease partly through the brain's innate immune system, where microglia drive most of the inflammation. It suggests this APOE effect is "likely linked" to TREM2, a receptor on microglia, but presents this as a hypothesis, and it reports no treatment, test or prevention.
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Our study demonstrated the robustness of a multisite Centiloid [ 11 C]PIB‐PET study and established a range of pathology‐based CL thresholds.
Why it matters
In 179 people across four centers, amyloid PET values on the Centiloid scale measured before death rose with the amount of plaque found at autopsy. A threshold of 12.2 Centiloids detected moderate-to-frequent plaques, and 24.4 identified intermediate-to-high Alzheimer's brain changes.
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Concluding, this innovative EEG analysis, in combination with a genetic test (both low-cost and widely available), could evaluate on an individual basis with great precision the risk of MCI progression.
Why it matters
In this study, combining EEG network measures with Apo-E genotyping discriminated amnestic MCI subjects who converted to Alzheimer dementia from those who stayed stable with 91.7% accuracy. This suggests a low-cost combination of tests could help estimate an individual's risk of progressing from MCI to dementia, though the findings need confirmation in larger groups.
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Altered proteome profiles have been reported in both postmortem brain tissues and body fluids of subjects with Alzheimer disease (AD), but their broad relationships with AD pathology, amyloid pathology, and tau-related neurodegeneration have not yet been fully explored.
Why it matters
This cross-sectional analysis measured hundreds of CSF proteins in 120 older adults with normal or impaired cognition to explore their association with core Alzheimer's pathology markers. It is a biomarker discovery study and does not test any treatment, cure, or prevention.
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Sex differences in Alzheimer's disease (AD) biology and progression are not yet fully characterized.
Why it matters
Among people with mild cognitive impairment due to Alzheimer's disease, cognitive worsening over up to 10 years was significantly greater in females than in males. This highlights the need to investigate sex differences further and develop sex-specific timelines for Alzheimer's progression.
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These results support the feasibility of bridging of clinical trials in the prodromal stage of AD between Asia and western countries.
Why it matters
Using the same enrolment criteria as North America's ADNI, the Japanese J-ADNI study found that people with amyloid-positive late amnestic mild cognitive impairment declined in "remarkably similar" ways in both regions (75 Japanese vs 269 North American participants), while decline in mild Alzheimer's disease was milder in the Japanese group (73 vs 230). Amyloid positivity was similar between regions in MCI and mild AD but higher among cognitively normal ADNI participants. The authors say this supports the "feasibility" of running early-stage (prodromal) Alzheimer's trials across Asia and Western countries; the study tested no treatment.
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The AD drug development pipeline is slightly larger in 2018 than in 2017.
Why it matters
As of January 30, 2018, there were 112 agents in the Alzheimer's disease treatment pipeline, with 63% being disease-modifying therapies. Amyloid biomarkers were used as entry criterion in 14 phase III disease-modifying agent trials and 17 disease-modifying agent trials in phase II.
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Biomarkers useful for the predementia stages of Alzheimer's disease are needed.
Why it matters
In 28 people with mild cognitive impairment and 38 cognitively normal people, resting-state MEG signals showed regional patterns linked to amyloid-beta deposition and other disease features. This is a small biomarker study and does not show that any treatment, cure, or prevention works.
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Plasma pTau181 may have utility as a biomarker of AD pathophysiology and as a noninvasive screener for elevated brain Aβ.
Why it matters
Among 172 cognitively unimpaired people, 57 with mild cognitive impairment and 40 with Alzheimer's dementia, blood levels of phospho-tau181 were higher in dementia and more strongly associated with amyloid and tau PET scans than total tau. The authors suggest plasma pTau181 may be useful as a noninvasive screen for elevated brain amyloid.
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Many genetic studies for Alzheimer's disease (AD) have been focused on the identification of common genetic variants associated with AD risk and not on other aspects of the disease, such as age at onset or rate of dementia progression.
Why it matters
Using longitudinal clinical data, this study tested whether the genetic architecture of Alzheimer's dementia progression differs from that of Alzheimer's risk, and found progression was not simply explained the same way. It reports no treatment, cure or prevention.
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Alzheimer's disease (AD) is a progressive neurodegenerative disorder that is characterized by cognitive decline and the presence of two core pathologies, amyloid β plaques and neurofibrillary tangles.
Why it matters
Reviews evidence that a sustained immune response in the brain, involving microglia and other immune cells, has emerged as a third core feature of Alzheimer's alongside amyloid plaques and tangles. It also covers how risk factors for Alzheimer's may relate to inflammation.
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Alzheimer disease (AD) is one of the most common diseases among the older adults.
Why it matters
This is a protocol for testing reminiscence therapy added to usual drug therapy in mild-to-moderate Alzheimer's disease. No results are reported, so its effect on cognition or other outcomes is not yet known.
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Neuropsychiatric symptoms (NPSs) are hallmarks of Alzheimer's disease (AD), causing substantial distress for both people with dementia and their caregivers, and contributing to early institutionalization.
Why it matters
This review describes neuropsychiatric symptoms as hallmarks of Alzheimer's disease that cause substantial distress and contribute to early institutionalization, and notes they are under-recognized and often challenging to treat. It discusses the neurobiology of these symptoms and clinical trial designs and regulatory considerations for developing treatments.
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Alzheimer's disease (AD) is a highly heritable complex disease with no current effective prevention or treatment.
Why it matters
This 2017 review reports that gene network analyses find immune networks "enriched in AD," and that many of these genes lie in genomic regions with common and rare variants associated with higher Alzheimer's risk. It notes that several of them — including CR1, SPI1, the MS4As, TREM2, ABCA7, CD33 and INPP5D — are expressed by microglia, the brain's resident immune cells, and suggests that such less-explored pathways "may be more fruitful targets for drug development" than the amyloid cascade alone. It is a review of association findings with no new data, and it does not report a treatment, cure or prevention.
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In all 6 patients (3 women and 3 men; mean age 61.8 years), the underlying clinical phenotype was associated with the regional distribution of the [18F]AV-1451 signal.
Why it matters
In six patients, the clinical phenotype matched the regional distribution of the tau PET signal, and cortical atrophy correlated strongly with tau binding. This supports tau PET as a marker linking tau pathology to neurodegeneration, but the study was very small and tested no treatment.
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Alzheimer's disease (AD) is the sixth leading cause of death in the United States and the most common cause of dementia in the elderly.
Why it matters
This 2017 review pulls together early research on TREM2, a gene active in the brain's immune cells (microglia), where rare variants "strongly impact the lifetime risk of developing AD." It summarises mouse studies suggesting TREM2 shapes how the brain's immune system responds to amyloid, and human spinal-fluid studies in which soluble TREM2 rises around the time of nerve-cell damage and dementia onset. It is a summary of others' work, not new evidence; it tests no treatment and does not show that changing TREM2 helps people.
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Soluble oligomers of amyloid β-protein (oAβ) isolated from the brains of Alzheimer's disease (AD) patients have been shown experimentally (in the absence of amyloid plaques) to impair hippocampal synaptic plasticity, decrease synapses, induce tau hyperphosphorylation and neuritic dystrophy, activate microglial inflammation, and impair memory in normal adult rodents.
Why it matters
Large soluble amyloid-β oligomers from Alzheimer brains had little or no cytotoxic activity, but dissociated into smaller oligomers that were far more neuroactive. This laboratory finding suggests that the size of amyloid-β oligomers matters, but it does not test or establish any treatment for patients.
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54/100
We selected 111 patients with probable DLB and CSF available from the Amsterdam Dementia Cohort.
Why it matters
In 111 people with probable dementia with Lewy bodies from the Amsterdam Dementia Cohort, 42 (38%) had spinal-fluid markers typical of Alzheimer's disease (CSF tau/Aβ42 ratio >0.52). The authors compared these patients with the rest on symptoms, thinking skills, nursing-home admission and survival, and their title reports that the added Alzheimer pathology "affects clinical manifestation and survival." It is an observational single-cohort study and does not test any treatment, cure or prevention.
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Moreover, the presence of Aβ+ was associated with an elevated [18F]-AV-1451 SUVR in AD cortical signature regions (Aβ+ participants: mean [SD], 1.3 [0.3]; Aβ- participants: 1.1 [0.1]; F = 4.3, P = .04) but not in the hippocampus.
Why it matters
In 59 participants, this tau imaging study found that elevated amyloid was linked to higher tau signal in certain cortical regions but not the hippocampus, and higher tau signal was linked to tissue loss in the hippocampus and cortex. It is an imaging study only and does not test any treatment, cure or prevention for Alzheimer's disease.
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Tau PET imaging with (18)F-AV-1451 could serve as an in vivo biomarker for the evaluation of AD-related tau pathology and monitoring disease progression.
Why it matters
In 20 Alzheimer patients, 15 with mild cognitive impairment, and 20 controls, tau PET binding was increased only in the entorhinal cortex in mild cognitive impairment and more widespread in Alzheimer disease, and it correlated with memory and atrophy. This is an observational imaging study and does not test any treatment or show that reducing tau would help.
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This common ABCA7 deletion could represent an ethnic-specific pathogenic alteration in AD.
Why it matters
A 44-base pair deletion in the ABCA7 gene was linked to Alzheimer's in African Americans (odds ratio 1.81 across two groups after adjusting for age, sex and APOE). It is predicted to disrupt the ABCA7 protein. It was common in African Americans (15.2% of cases, 9.74% of controls) but found in only 0.12% of the study's non-Hispanic white cohort, which suggests an ancestry-specific risk factor. This is an association: many carriers did not have the disease, and the study does not show a treatment, prevention or test.
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When poor SRH was present we found no increased risk for NH placement or death among elderly people with mild AD.
Why it matters
In 321 home-living elderly people with mild Alzheimer's disease, poor self-rated health was not linked to increased risk of nursing home placement or death over three years. This concerns prediction of these outcomes, not treating, curing, or preventing the disease.
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Recent studies highlight the implication of innate and adaptive immunity in the pathophysiology of Alzheimer's disease, and foster immunotherapy as a promising strategy for its treatment.
Why it matters
In APPPS1 mice, a mouse model of Alzheimer-like disease, briefly removing regulatory T cells early in life made memory and thinking problems appear sooner, even though amyloid-β deposits did not change. This suggests these immune cells influence how the disease progresses in mice, separately from amyloid buildup. It is animal work only: the authors were motivated by the serious T-cell-related side effects in the AN1792 vaccine trial, and nothing here tests a treatment in people.
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In this study, we update the TDP-43 in Alzheimer's disease staging scheme by assessing the topography of TDP-43 in 193 cases of Alzheimer's disease, in 14 different brain regions (eight previously described plus six newly reported) and use conditional probability to model the spread of TDP-43 across the 14 brain regions.
Why it matters
In 193 Alzheimer's disease cases, TDP-43 was found in 14 brain regions and a conditional probability analysis produced six stages of spread beginning in the amygdala. This updated staging scheme classifies cases and shows clinical significance but reports no 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.
- Down syndrome, Alzheimer's disease and seizures
- Inflammation context in Alzheimer's disease, a relationship intricate to define
- Reduced hippocampal functional connectivity in Alzheimer disease
- Processing of Alzheimer beta/A4 amyloid precursor protein: modulation by agents that regulate protein phosphorylation
- Very mild Alzheimer's disease: informant-based clinical, psychometric, and pathologic distinction from normal aging
- Novel white matter tract integrity metrics sensitive to Alzheimer disease progression
- The role of innate immune genes in Alzheimer's disease
- Mitochondrial Dysfunction and Alzheimer's Disease: Role of Microglia
- Inflammation in Alzheimer's Disease and Molecular Genetics: Recent Update
- Accuracy of Biomarker Testing for Neuropathologically Defined Alzheimer Disease in Older Adults With Dementia