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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At baseline measurements, amyloid burden does not distinguish between cognitively impaired and unimpaired subjects with PD without dementia, but our data suggest that amyloid contributes to cognitive, but not motor, decline over time.
Why it matters
In this small cohort of 46 people with Parkinson disease without dementia, baseline amyloid burden did not distinguish those with mild cognitive impairment from those with normal cognition, but higher amyloid retention predicted conversion to a more severe diagnosis. It is an early observational finding in Parkinson disease and does not test a treatment, cure, or prevention for Alzheimer's disease.
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44 participants were included: 20 PSEN1 E280A mutation carriers and 24 non-carriers.
Why it matters
In 44 Colombians aged 18–26 from one family (20 carrying the PSEN1 E280A mutation, which causes early-onset Alzheimer's disease, and 24 non-carriers), carriers showed brain-scan and spinal-fluid/blood differences that the authors describe as "consistent with Aβ(1-42) overproduction," including greater right hippocampal and parahippocampal activation during a memory task, even though the two groups did not differ on dementia ratings or thinking tests. The authors call these "the earliest known biomarker changes in cognitively normal people" at genetic risk for this inherited form of Alzheimer's, but say it is still undetermined whether the changes are "neurodegenerative or developmental." It is a single-timepoint comparison in one mutation-carrying family and tested no treatment.
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This study provides initial data that demonstrate elevated antibodies to periodontal disease bacteria in subjects years before cognitive impairment and suggests that periodontal disease could potentially contribute to the risk of AD onset/progression.
Why it matters
In 158 people who were cognitively intact at the start, higher serum antibody levels to the periodontal bacterium Fusobacterium nucleatum were found in those who later developed Alzheimer's disease or mild cognitive impairment. This links a marker of periodontal infection to later cognitive decline, but it does not show that treating gum disease would prevent or cure Alzheimer's disease.
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A consensus panel from the United States and Europe was convened recently to update and revise the 1997 consensus guidelines for the neuropathologic evaluation of Alzheimer's disease (AD) and other diseases of brain that are common in the elderly.
Why it matters
A US–European consensus panel revised the 1997 guidelines for examining the brain after death for Alzheimer's disease. The update recognises a "pre-clinical stage" of the disease and assesses amyloid build-up as well as neurofibrillary change and neuritic plaques. It also sets protocols for Lewy body disease, vascular brain injury, hippocampal sclerosis and TDP-43 inclusions, and recommends standard ways to compare brain findings with a person's symptoms in life. These are standards for pathologists and researchers, not a test, treatment or prevention.
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Naproxen may attenuate cognitive decline in slow decliners while accelerating decline in fast decliners.
Why it matters
This re-analysis of 2,388 participants in the Alzheimer's Disease Anti-inflammatory Prevention Trial used how fast people's 3MS cognitive test scores fell as a stand-in for how far pre-clinical Alzheimer's had progressed, and found three groups: no, slow and fast decline. The authors report that naproxen "may attenuate cognitive decline in slow decliners while accelerating decline in fast decliners," while celecoxib "appeared to have similar effects at first but then attenuated change in fast decliners." They call these contrasts "unexpected," so the study suggests that drug effects may differ by disease phase; it does not show that anti-inflammatory drugs protect against Alzheimer's.
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Recent GWAS studies focused on uncovering novel genetic loci related to AD have revealed associations with variants near CLU, CR1, PICALM and BIN1.
Why it matters
This genome-wide association study in 1034 cases and 1186 controls, combined with other datasets, replicated associations near PICALM and CR1 and identified variants at the BIN1 locus linked to late-onset Alzheimer's disease. It identifies genetic risk factors but does not provide a treatment, cure or prevention.
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Aβ deposition increases slowly from cognitive normality to moderate severity DAT.
Why it matters
In 206 people (35 with Alzheimer's dementia, 65 with mild cognitive impairment, 106 healthy controls) given repeat amyloid PET scans about 20 months apart, amyloid rose slightly in the dementia and MCI groups and in healthy people who already had high amyloid, and the rise was associated with the number of APOE ε4 alleles. People with mild cognitive impairment and high amyloid progressed to Alzheimer's dementia far more often than those with low amyloid (67% vs 5%), and 25% of healthy controls with high amyloid developed impairment by 3 years. But the link between rising amyloid and cognitive decline was weak, and 20% of low-amyloid MCI patients developed other dementias, so a scan result is a risk signal, not a diagnosis. The study describes no treatment.
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Poor vitamin D nutrition is linked with dementia, but vitamin D has not been tested in a randomized controlled trial (RCT) in Alzheimer's disease (AD).
Why it matters
This small randomized trial gave high-dose vitamin D followed by nasal insulin to 32 people with mild to moderate Alzheimer's disease. It does not report that this combination prevents or cures Alzheimer's disease.
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We used a new method of pooling cerebrospinal fluid Aβ42 and Pittsburgh compound B positron emission tomography measures to produce equivalent measures of brain Aβ load from either source and analysed the results using multiple imputation methods.
Why it matters
Among people with mild cognitive impairment, those who tested amyloid-positive (by spinal-fluid test or PET scan, pooled onto one scale) were much more likely to progress to dementia within 2 years than those who tested negative — 50% versus 19%. Above high levels, having more amyloid did not further raise the risk, which the authors say is "consistent with" amyloid starting the disease process rather than directly causing the memory and thinking problems. This is a prediction study, not a treatment study, and although the title also names MRI atrophy as a predictor, the summary gives no MRI result.
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Cognitive decline associated with Parkinson disease (PD) is common and highly disabling.
Why it matters
In 45 patients with Parkinson disease followed longitudinally, cerebrospinal fluid amyloid β 1-42 predicted cognitive decline. This is a Parkinson disease study, so it does not provide evidence about treating, curing or preventing Alzheimer's disease.
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63/100
Increased amygdalar diffusivity in the absence of tissue loss in dementia with Lewy bodies (DLB) may be related to microvacuolation, a common pathology associated with Lewy body disease in the amygdala.
Why it matters
This case-control imaging study found different patterns of brain tissue changes in dementia with Lewy bodies versus Alzheimer disease, with amygdala changes in DLB possibly related to microvacuolation. It does not test any treatment, cure, or prevention, and only suggests that diffusion MRI may add information beyond standard structural scans.
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Vascular care in patients with Alzheimer disease with cerebrovascular lesions slows progression of WMLs.
Why it matters
In people with Alzheimer's disease who also had cerebrovascular lesions on MRI, multicomponent vascular care slowed progression of white matter lesions compared with standard care, but there was no difference in new lacunes or in global cortical or medial temporal lobe atrophy. This addresses a vascular target in dementia rather than curing or preventing Alzheimer's disease itself.
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Disease modifying drugs for Alzheimer's disease (AD) are likely to be most effective when given in non-demented subjects.
Why it matters
This review and meta-analysis summarized CSF and blood biomarkers that predict conversion from mild cognitive impairment to Alzheimer-type dementia and examined whether they could reduce sample size and costs in prevention trials. It is a methodological review and does not itself test any treatment, cure, or prevention.
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Brain atrophy with aging was observed in supratentorial and infratentorial areas, as well in primary motor, sensory, and heteromodal association regions.
Why it matters
Comparing 169 cognitively normal people and 33 with probable Alzheimer disease, normal aging and Alzheimer disease showed overlapping atrophy in the hippocampal body and entorhinal cortex but also distinct patterns. This is a structural imaging comparison and does not test any treatment or prevention.
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Tensor-based morphometry can recover three-dimensional longitudinal brain changes over time by nonlinearly registering baseline to follow-up MRI scans of the same subject.
Why it matters
In this one-year follow-up of 20 Alzheimer's disease patients, 40 controls, and 40 with mild cognitive impairment, widespread cerebral atrophy was detected in Alzheimer's disease and a more restricted pattern in mild cognitive impairment, with temporal lobe atrophy faster in those who converted. Atrophy rates correlated with clinical measures and biomarkers, but no treatment or prevention is tested.
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63/100
Enrollment began in March 2001 and ended in December 2004 when treatments were suspended because of concerns regarding cardiovascular safety of the treatments.
Why it matters
This paper describes the design of a prevention trial testing whether the anti-inflammatory drugs celecoxib or naproxen could prevent Alzheimer's disease in people aged 70 and older with a family history of dementia. The trial enrolled 2,528 participants but treatments were suspended early because of concerns about cardiovascular safety, so it did not provide answers about prevention.
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Researchers extracted soluble amyloid-beta protein oligomers directly from the cerebral cortex of subjects with Alzheimer's disease to study their impact.
Why it matters
Reports that amyloid-beta protein dimers taken directly from Alzheimer's brains impaired synaptic plasticity and memory.
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Apathy is a common behavioral symptom of Alzheimer's disease (AD), being present in up to 70% of patients.
Why it matters
In this small crossover trial of 13 patients with apathy in Alzheimer disease, methylphenidate produced greater improvement on apathy scores than placebo, but significantly more patients had at least one adverse event with methylphenidate, including two serious events. This is a small study about treating apathy as a symptom, not about curing or preventing Alzheimer's disease.
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63/100
Risk information for Alzheimer disease (AD) may be communicated through susceptibility gene disclosure, even though this is not currently in clinical use.
Why it matters
In this randomized trial, people who learned they were APOE epsilon4 positive were more likely to report Alzheimer-specific health behavior changes one year later than those who learned they were epsilon4 negative. Participants were told no proven preventive measures for Alzheimer disease existed, so the study concerns behavior after risk disclosure, not a treatment or cure.
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63/100
From a longitudinal study of normal (Clinical Dementia Rating [CDR] = 0; n = 77) and mildly impaired (CDR = 0.5; n = 167) participants with 5 or more annual clinical assessments, baseline level of cognitive impairment in daily life was graded using CDR sum of boxes (CDR-SB) and level of cognitive performance impairment was graded using neuropsychological test scores.
Why it matters
This longitudinal study looked at whether grading the severity of mild cognitive impairment can predict who will later be diagnosed with Alzheimer's disease dementia. It is about improving prediction of decline, not about treating, curing or preventing the disease.
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Distinguishing Alzheimer's disease (AD) and frontotemporal dementia (FTD) currently relies on a clinical history and examination, but positron emission tomography with [(18)F] fluorodeoxyglucose (FDG-PET) shows different patterns of hypometabolism in these disorders that might aid differential diagnosis.
Why it matters
In 45 patients whose diagnosis was later confirmed by brain tissue (31 Alzheimer's, 14 frontotemporal dementia), six dementia experts chose between the two diagnoses more reliably and accurately from FDG-PET brain-metabolism maps (89.6% accuracy) than from clinical information alone, and adding the scan to a clinical summary helped most when they were unsure. The study only compared these two diagnoses, used expert readers and a small FTD group, and is a diagnostic aid — it does not treat, cure or prevent Alzheimer's disease.
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63/100
The NINCDS-ADRDA and the DSM-IV-TR criteria for Alzheimer's disease (AD) are the prevailing diagnostic standards in research; however, they have now fallen behind the unprecedented growth of scientific knowledge.
Why it matters
This proposal revised the diagnostic criteria for Alzheimer's disease to capture the earliest stages before full-blown dementia, centering on early and significant episodic memory impairment plus at least one abnormal biomarker from MRI, PET, or cerebrospinal fluid analysis of amyloid beta or tau proteins. The authors note that validation studies are needed to optimize the criteria's sensitivity, specificity, and accuracy.
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Thirty percent of the cases had significant cerebrovascular parenchymal pathology scores (CVDPS), 54% had significant AD pathology, and 18% had HS.
Why it matters
In 79 autopsy cases from a long-term study of subcortical ischemic vascular disease and Alzheimer's, 30% had significant vascular tissue damage, 54% significant Alzheimer's pathology and 18% hippocampal sclerosis. In the authors' analysis each of the three contributed independently to cognitive status, but only the Alzheimer's staging measure (Braak and Braak stage) contributed to a global neuropsychological measure of impairment. These are associations in brains examined after death; the study did not test any treatment, and its APOE findings are not included in this record.
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Hyperinsulinemia is associated with a higher risk of AD and decline in memory.
Why it matters
In 683 people aged 65 and older from northern Manhattan who did not have dementia at the start, those with high fasting insulin (39% of the group) went on to develop Alzheimer's disease at about twice the rate of the others (hazard ratio 2.1, 95% CI 1.5–2.9), and the link was strongest in people without diabetes. High insulin was also tied to faster decline in memory scores, but not in other thinking skills. This is an observational association: the study did not test whether lowering insulin changes anyone's risk.
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This report describes the first human study of a novel amyloid-imaging positron emission tomography (PET) tracer, termed Pittsburgh Compound-B (PIB), in 16 patients with diagnosed mild AD and 9 controls.
Why it matters
In this first human study of the amyloid-imaging PET tracer Pittsburgh Compound-B, 16 patients with mild Alzheimer's disease showed marked retention of the tracer in areas of association cortex known to contain large amounts of amyloid deposits, compared with 9 controls. The results suggest that PET imaging with this tracer can provide quantitative information on amyloid deposits in living subjects.
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.
- Machine Learning Models of Polygenic Risk for Enhanced Prediction of Alzheimer Disease Endophenotypes
- Default-mode network activity distinguishes Alzheimer's disease from healthy aging: Evidence from functional MRI
- COVID-19 and Alzheimer's disease: how one crisis worsens the other
- Role of RAGE in Alzheimer's Disease
- Survival and mortality differences between dementia with Lewy bodies vs Alzheimer disease
- A new rating scale for Alzheimer's disease
- Analyzing heterogeneity in Alzheimer disease using multimodal normative modeling on imaging‐based ATN biomarkers
- ADCOMS: a composite clinical outcome for prodromal Alzheimer's disease trials
- Defined neurofilament, tau, and beta-amyloid precursor protein epitopes distinguish Alzheimer from non-Alzheimer senile plaques
- Caregivers' judgments of the functional abilities of the Alzheimer's disease patient: a comparison of proxy reports and objective measures