Each study has a usefulness score out of 100 (rubric version 4.0). Tap a score to see what makes it up.
Highest usefulness score first. Studies without a score come last.
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Increased Aβ burden was observed in TBI.
Why it matters
In this small study of 28 participants, long-term survivors of traumatic brain injury showed increased β-amyloid binding in the posterior cingulate cortex and cerebellum compared with controls. The distribution overlapped with but was distinct from Alzheimer disease, so this does not show that traumatic brain injury causes Alzheimer's disease.
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52/100
Low CSF Aβ1-42 may be a significant predictor of POCD at 3 months.
Why it matters
In this small study of older hip replacement patients, low CSF Aβ1-42 was linked to a higher rate of postoperative cognitive dysfunction at 3 months, while the other analytes showed no significant difference. This suggests a possible risk marker for cognitive problems after surgery, but it does not test a treatment, cure, or prevention for Alzheimer's disease.
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Despite its potential benefits, few published studies have explored the advantages or risks of a timely diagnosis of AD.
Why it matters
This review searched studies published from 2000 to mid-2014 and found only nine that looked at what happens after Alzheimer's is diagnosed early, and none focused on the stage before dementia. It lists possible gains from a timely diagnosis, such as coordinated care plans, better symptom management, patient safety and delaying a move into care, but these are presented as potential benefits rather than measured results. It also names barriers: stigma, suicide risk, lack of clinician training, diagnostic uncertainty, too few specialist services, and doctors' reluctance to diagnose when no disease-modifying treatment exists.
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Type 2 diabetes (T2DM), Alzheimer's disease (AD), and insulin resistance are age-related conditions and increased prevalence is of public concern.
Why it matters
This review links type 2 diabetes, insulin resistance, chronic inflammation and oxidative stress to Alzheimer's disease through shared molecular features. It does not report any treatment or cure, and its suggestions about common mechanisms remain to be tested in trials.
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Amyloid-PET-based CSF Aβ42 cutpoints were higher and tended to reduce intercenter variability compared with clinical-based cutpoints.
Why it matters
Across 433 people at 5 European centers, spinal-fluid amyloid (CSF Aβ42) cut-offs set against amyloid PET scans were higher (521–616 pg/mL) than the cut-offs clinics were using (400–550 pg/mL), and they varied less from center to center. At the pooled cut-off of 557 pg/mL, the fluid test and the scan agreed for 84% of participants, so roughly 1 in 6 got a different answer from each test. This is a diagnostic study. It does not report any treatment, cure or prevention of Alzheimer's disease.
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Down syndrome, which arises in individuals carrying an extra copy of chromosome 21, is associated with a greatly increased risk of early-onset Alzheimer disease.
Why it matters
This review explains that Down syndrome, caused by an extra copy of chromosome 21, is associated with a greatly increased risk of early-onset Alzheimer disease, thought to be conferred by three copies of the APP gene. It suggests studying these mechanisms could give insight into dementia in the general population, but reports no treatment, cure or prevention.
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Disturbances in the sleep-wake cycle and circadian rhythms are common symptoms of Alzheimer Disease (AD), and they have generally been considered as late consequences of the neurodegenerative processes.
Why it matters
This review discusses how sleep-wake and circadian disruption often occur early in Alzheimer's disease and may even precede cognitive symptoms. The sleep-wake cycle appears to regulate levels of amyloid-beta peptide in the brain, and manipulating sleep can influence Alzheimer's-related pathology in mouse models.
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Common single nucleotide polymorphisms in the SORL1 gene have been associated with late onset Alzheimer disease (LOAD), but causal variants have not been fully characterized nor has the mechanism been established.
Why it matters
This family- and cohort-based genetic association study identified coding mutations in the SORL1 gene in patients with late-onset Alzheimer's disease. It is genetic research and does not test any treatment, cure, or prevention.
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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.
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.
- Cognitive Phenotyping and Interpretation of Alzheimer Blood Biomarkers
- Voxelwise meta-analysis of gray matter anomalies in Alzheimer's disease and mild cognitive impairment using anatomic likelihood estimation
- Contributions of brain insulin resistance and deficiency in amyloid-related neurodegeneration in Alzheimer's disease
- The neuropathological diagnosis of Alzheimer's disease
- Amyloid imaging and CSF biomarkers in predicting cognitive impairment up to 7.5 years later
- Optimization of Statistical Single Subject Analysis of Brain FDG PET for the Prognosis of Mild Cognitive Impairment-to-Alzheimer's Disease Conversion
- Blood-derived mitochondrial DNA copy number is associated with Alzheimer disease, Alzheimer-related biomarkers and serum metabolites
- Clarifying the association of CSF Aβ, tau, BACE1, and neurogranin with AT(N) stages in Alzheimer disease
- MRI biomarkers of vascular damage and atrophy predicting mortality in a memory clinic population
- Alzheimer-type dementia and verbal memory performances: influence of selegiline therapy