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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Key experiments using fibril-free AβO solutions demonstrated that while Aβ is essential for memory loss, the fibrillar Aβ in amyloid deposits is not the agent.
Why it matters
This review argues that amyloid β oligomers, rather than fibrillar amyloid in deposits, provide a molecular basis for the cause, treatment, and diagnosis of Alzheimer's disease. It is a summary of evidence and does not report a proven treatment, cure, or prevention.
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Reported rates of dementia differ by race, although most studies have not focused on carefully measured outcomes, confounding by education or other demographic factors, nor have they studied other outcomes other than dementia.
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The derived threshold was used to categorize the 172 scans in the test cohort as negative or positive, and results were compared with categorization using visual assessment.
Why it matters
An automated, PET-only method sorted 18F-flutemetamol amyloid scans into negative or positive and showed "a strong concordance with visual read results" and "good agreement with histopathologic classification of neuritic plaque density". Using the pons as the reference region, it reached 91% sensitivity and 88% specificity, with 3 false-positive and 4 false-negative scans in a 172-scan test cohort. It is a tool for reading amyloid scans consistently, not a diagnosis of dementia and not a treatment.
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Hypometabolism in PiB-positive, cognitively normal subjects in a population-based cohort occurs in AD-signature cortical regions and to a lesser extent in other cortical regions.
Why it matters
In cognitively normal older adults, lower brain metabolism in Alzheimer-related regions was linked to higher amyloid levels on PET scans. This supports using metabolism scans alongside amyloid scans in studies of early Alzheimer disease, but it does not show that treating hypometabolism prevents dementia.
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Building infrastructures for international collaborations is necessary for managing the worldwide public health problem of AD and dementia.
Why it matters
This review discusses the shift toward presymptomatic and pre-dementia stages of Alzheimer's disease and notes that associations between neuropathology and cognition are still not entirely clear. It describes ongoing intervention studies and methodological issues but does not report results from a prevention trial.
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The increase in life expectancy has resulted in a high occurrence of dementia and Alzheimer's disease (AD).
Why it matters
This paper describes risk scores that may help identify people at higher risk of dementia who could benefit from interventions, and it describes ongoing prevention trials. It reports no results on whether any treatment prevents or cures Alzheimer's disease.
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Factors other than age and genetics may increase the risk of developing Alzheimer disease (AD).
Why it matters
In experimental models, this review reports, sleep deprivation raised soluble amyloid-β and led to its chronic build-up, while extra sleep had the opposite effect. It also describes the reverse: once amyloid-β accumulates, wakefulness increases and sleep patterns change, and people with early amyloid deposits but normal thinking "report sleep abnormalities". The authors conclude sleep and Alzheimer's "may influence each other". The record contains no human trial, numbers or tested treatment.
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The amyloid cascade hypothesis is widely accepted as the centerpiece of Alzheimer disease (AD) pathogenesis.
Why it matters
This 2013 review argues that amyloid alone can't explain Alzheimer's: lab studies show amyloid is toxic only at "micromolar concentrations," while levels in the brain are "a million times lower." The authors propose instead that the brain's inflammatory response to amyloid deposits, later amplified by tau, "probably" drives the disease, and they cite population and animal studies linking anti-inflammatory NSAIDs to a "sparing effect" as proof of concept, which is not evidence from clinical trials. They also note biomarker evidence that the disease starts "more than a decade before it becomes clinically evident," so treatment may need to begin early.
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52/100
Deposition of insoluble protein aggregates is a hallmark of neurodegenerative diseases.
Why it matters
In brain tissue, U1 snRNP spliceosome components accumulated in Alzheimer's disease and were already present in mild cognitive impairment, with unspliced RNA species building up. This identifies a possible disease process but does not test any treatment, cure or prevention.
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As one of the first attempts to use an imaging technique that does not require amyloid-specific radioligands for identification of individuals with brain amyloidosis, our findings could lead to development of multidisciplinary/multimodality brain amyloidosis biomarkers that are reliable, minimally invasive, and widely available.
Why it matters
A structural MRI-based score, combined with APOE genotype, predicted which people with mild cognitive impairment were likely to have high brain amyloid better than either measure alone. This is about screening who might have amyloid, not about treating, curing or preventing Alzheimer's disease.
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Computational anatomy with magnetic resonance imaging (MRI) is well established as a noninvasive biomarker of Alzheimer's disease (AD); however, there is less certainty about its dependency on the staging of AD.
Why it matters
Using existing MRI scans from the Alzheimer's Disease Neuroimaging Initiative, a machine-learning classifier picked out Alzheimer's-type brain changes in people with mild cognitive impairment about 4 years before they developed dementia. Its performance was "significantly above the chance level (62%)", which is a research signal, not a reliable test for an individual. The authors also found that the pattern of brain shrinkage differed between Alzheimer's patients the computer classified correctly and those it missed, which "challenges the assumption of a uniform pathophysiological process" behind clinically diagnosed Alzheimer's. The study tested no treatment.
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Diffusion tensor imaging (DTI) based assessment of white matter fiber tract integrity can support the diagnosis of Alzheimer's disease (AD).
Why it matters
Machine learning classification of diffusion tensor imaging data from multiple scanners achieved up to 83% accuracy in distinguishing Alzheimer's disease patients from healthy controls. This supports the use of DTI as a diagnostic biomarker and does not treat, cure, or prevent Alzheimer's disease.
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A large proportion of subjects with AD dementia in ADNI may be categorized more definitively as high-probability AD using the proposed biomarker scheme in the NIA-AA criteria.
Why it matters
Applying the NIA-AA biomarker criteria to 211 people with Alzheimer's dementia from ADNI, 87% could be classified as high-probability Alzheimer's disease when requiring a positive amyloid biomarker and one neuronal injury marker. A minority could be classified as dementia unlikely due to Alzheimer's, showing that the criteria can categorize most but not all cases.
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Dementia is a global epidemic with Alzheimer's disease (AD) being the leading cause.
Why it matters
This study developed a nine-marker blood test that predicted high brain amyloid burden with about 80% sensitivity and specificity, validated in a second group. It is a step toward a population screening tool, not a treatment, cure or prevention.
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Microglial cells closely interact with senile plaques in Alzheimer's disease and acquire the morphological appearance of an activated phenotype.
Why it matters
In two mouse models of Alzheimer's disease, microglial process motility and phagocytic activity were impaired alongside amyloid deposition. This is animal research and does not show any treatment, cure or prevention for people.
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Increased awareness of cognitive and behavioural change in amyotrophic lateral sclerosis has been driven by various clinic-based and population-based studies.
Why it matters
This review describes cognitive and behavioural changes in ALS, including impairments that overlap with frontotemporal dementia, and calls for better assessment tools. It does not test any treatment or prevention for Alzheimer's disease, so it has no direct implications for treating, curing, or preventing the disease.
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We found no evidence of acceleration in whole-brain atrophy rates in any group.
Why it matters
In this imaging study, whole-brain atrophy rates did not accelerate in any group, but hippocampal atrophy rates accelerated in people with mild cognitive impairment, driven by those who progressed to Alzheimer disease. This describes atrophy patterns over time and does not test a treatment.
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For example, focal temporal lobe dysfunction is associated with a pure amnestic syndrome, very slow decline, with atrophy and neurofibrillary tangles limited largely to the medial temporal region including the entorhinal cortex.
Why it matters
Alzheimer's disease is not one uniform condition: different brain regions affected produce different symptoms, ages of onset, and rates of decline. Genotypic differences, such as absence of apolipoprotein E e4, may underlie some of these subtypes.
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Florbetapir F18 has been approved by the Food and Drug Administration for in vivo assessment of amyloid pathology in patients undergoing evaluation for Alzheimer disease (AD).
Why it matters
After receiving florbetapir F18 amyloid imaging results, diagnosis changed in 54.6% of patients undergoing evaluation for cognitive decline, and diagnostic confidence increased by an average of 21.6%. Intended treatment with cholinesterase inhibitors or memantine increased in patients with positive scans and decreased in those with negative scans.
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Although amyloid-beta (Aβ) peptide deposition into insoluble plaques is a pathological hallmark of Alzheimer disease; soluble oligomeric Aβ has been hypothesized to more directly underlie impaired learning and memory in dementia of the Alzheimer type.
Why it matters
A new single-molecule assay measured soluble amyloid beta oligomers, which are hypothesized to underlie impaired learning and memory in Alzheimer's dementia. This is a test-development study and does not by itself provide a treatment or cure.
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PiB and florbetapir retention ratios were strongly associated in the same individuals, and this relationship was consistent across several data analysis methods, despite scan-rescan intervals of more than a year.
Why it matters
In 32 ADNI participants scanned with both PiB and florbetapir amyloid PET, results from the two tracers were strongly associated across several analysis methods. The authors show that cutoffs for amyloid positive or negative status can be converted between the two tracers.
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Amyloid plaques and hyperphosphorylated tau in cortical brain biopsies are reflected by low CSF Aβ42 and high CSF tau and p-tau levels, respectively.
Why it matters
In patients who had brain biopsies, those with amyloid plaques or tau in the tissue tended to have lower Aβ42 and higher tau and p-tau 181 in their spinal fluid. This supports using spinal fluid markers to reflect brain changes, which aids diagnosis but does not treat or prevent the disease.
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Performing exome sequencing in 14 autosomal dominant early-onset Alzheimer disease (ADEOAD) index cases without mutation on known genes (amyloid precursor protein (APP), presenilin1 (PSEN1) and presenilin2 (PSEN2)), we found that in five patients, the SORL1 gene harbored unknown nonsense (n=1) or missense (n=4) mutations.
Why it matters
In people with autosomal dominant early-onset Alzheimer's disease without mutations in known genes, several potentially pathogenic SORL1 mutations were found and were absent from controls. This genetic finding links SORL1 to a rare inherited form of the disease but does not by itself provide a treatment or cure.
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Short-term nutritional supplements enable an improvement in Alzheimer patients' nutritional status, but it remains to be seen whether they will be sufficient to improve long-term nutritional status.
Why it matters
A 3-week nutritional supplement programme improved nutritional status scores in undernourished patients with mild probable Alzheimer's disease, and the improvement persisted at 90 days. This addresses nutrition, not the treatment, cure, or prevention of Alzheimer's disease itself.
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We explored resting-state metabolic connectivity in prodromal Alzheimer's disease (pAD) patients and in healthy controls (CTR), through a voxel-wise interregional correlation analysis of 18F-fluorodeoxyglucose (FDG)-positron emission tomography (PET) by means of statistical parametric mapping.
Why it matters
Patients with prodromal Alzheimer's disease showed less metabolic connectivity than controls in both hypometabolic and nonhypometabolic areas, including the hippocampi and dorsolateral prefrontal cortex. This reduced connectivity suggests that metabolic disconnection may occur before remote hypometabolism, an early sign of synaptic degeneration.
From across this topic
10 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 10. The same 10 appear here every time.
- A multiancestry polygenic risk score for Alzheimer's disease is associated with cognitive decline and neuropathological hallmarks in diverse populations
- Rofecoxib: no effect on Alzheimer's disease in a 1-year, randomized, blinded, controlled study
- N400 evidence of abnormal responses to speech in Alzheimer's disease
- Recent advances in neuroimaging of Alzheimer's disease and related dementias
- Automated detection of brain atrophy patterns based on MRI for the prediction of Alzheimer's disease
- Activities of key glycolytic enzymes in the brains of patients with Alzheimer's disease
- Fully automated measurement of plasma Aβ42/40 and p-tau181: Analytical robustness and concordance with cerebrospinal fluid profile along the Alzheimer's disease continuum in two independent cohorts
- Brain differences in infants at differential genetic risk for late-onset Alzheimer disease: a cross-sectional imaging study
- Rates of Alzheimer disease biomarker positivity stratified by by sex and race in a specialty memory clinic
- There Is No Direct Causal Relationship Between Coronary Artery Disease and Alzheimer Disease: A Bidirectional Mendelian Randomization Study