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.
-
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.
-
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.
-
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.
-
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.
-
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.
-
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.
-
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.
-
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.
-
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.
-
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.
-
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.
-
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.
-
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.
-
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.
-
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.
-
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.
-
Researchers derived a triple-transgenic model to study the interaction between Abeta and tau and their effect on synaptic function.
Why it matters
Describes a triple-transgenic model of Alzheimer's disease that develops both plaques and tangles. A disease model is a research tool for testing ideas and candidate treatments, and is not a treatment itself.
-
A high percentage of patients with mild cognitive impairment (MCI) develop clinical dementia of the Alzheimer type (AD) within 1 year.
Why it matters
In this one-year PET study of 22 people with mild cognitive impairment, the 8 who developed probable Alzheimer's already showed lower brain glucose use in temporoparietal and posterior cingulate regions at baseline; the posterior cingulate difference was significant even against those who stayed stable. Over the year, converters also developed a new drop in prefrontal areas that was not seen in the stable group. This is a small group-level association, not a test that predicts an individual's outcome and not a treatment.
-
Advances in genetic research have provided a basis for susceptibility testing for Alzheimer disease (AD).
Why it matters
This study examined why 206 adult children of people with Alzheimer's disease sought genetic susceptibility testing, with the most common reasons being to contribute to research, arrange personal affairs, and hope for effective treatment. The findings show interest in testing even without available treatments, but the study does not test any treatment, cure, or prevention for Alzheimer's disease.
-
Two hundred fifty-two patients (67 percent women; mean age, 76 years) from 32 U.S. centers were enrolled.
Why it matters
In a 28-week trial, patients with moderate-to-severe Alzheimer's taking memantine had better outcomes on some measures of daily living and overall change than those taking placebo. This suggests memantine may help with symptoms in later stages, but it does not cure or prevent the disease.
-
63/100
To characterize antibodies produced in humans in response to Abeta42 vaccination, we carried out immunohistochemical examinations of the brains of both transgenic mice and human patients with beta-amyloid pathology.
Why it matters
Patients with Alzheimer's disease who received an Abeta42 vaccination developed antibodies that recognized amyloid plaques, diffuse deposits and vascular amyloid without cross-reacting with normal amyloid precursor protein. This shows the vaccine could produce the intended antibodies but does not report whether it improved or prevented disease.
-
People with raised systolic blood pressure (≥160 mm Hg) or high serum cholesterol concentration (≥6.5 mmol/l) in midlife had a significantly higher risk of Alzheimer's disease in later life, even after adjustment for age, body mass index, education, vascular events, smoking status, and alcohol consumption, than those with normal systolic blood pressure (odds ratio 2.3, 95% confidence interval 1.0 to 5.5) or serum cholesterol (odds ratio 2.1, 1.0 to 4.4).
Why it matters
This longitudinal population study found that raised systolic blood pressure or high serum cholesterol in midlife was associated with a higher risk of Alzheimer's disease later in life, and having both risk factors increased the risk further. It does not test a treatment or cure, but suggests that managing these vascular risk factors in midlife might be relevant to prevention.
-
Studies conducted more than 20 years ago suggested that physostigmine could improve memory in people with or without dementia.
Why it matters
This review found that conventional oral physostigmine showed no benefit compared with placebo, while controlled-release physostigmine produced small improvements on two symptom measures in a group of identified responders. Physostigmine was also linked to significantly more patients withdrawing from trials and more side effects such as nausea and vomiting.
-
We examined the pattern of cognitive impairment and rate of cognitive and functional decline as a function of age at symptom onset in 127 patients with probable Alzheimer's disease (AD).
Why it matters
Among 127 patients with probable Alzheimer's disease, those with symptom onset before age 65 declined more rapidly over two years than those with later onset, even though both groups were similarly impaired at the start. This means age at symptom onset may help predict how fast the disease progresses, but it does not point to a treatment or cure.
-
The apolipoprotein E type 4 allele (APOE-epsilon 4) is genetically associated with the common late onset familial and sporadic forms of Alzheimer's disease (AD).
Why it matters
In 42 families with late onset Alzheimer's disease, risk for the disease increased from 20% to 90% and mean age at onset decreased from 84 to 68 years with increasing number of APOE-epsilon 4 alleles. The authors conclude that APOE-epsilon 4 gene dose is a major risk factor for late onset Alzheimer's disease, and in these families homozygosity was virtually sufficient to cause the disease by age 80.
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.
- 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
- Associations of Alzheimer Disease and Related Dementia Neuropathologies With Timely Diagnosis of Dementia in Healthcare Settings
- Mirtazapine for treatment of depression and comorbidities in Alzheimer disease
- PET staging of amyloidosis using striatum
- Animal models of Alzheimer's disease and frontotemporal dementia
- MRI Asymmetry Index of Hippocampal Subfields Increases Through the Continuum From the Mild Cognitive Impairment to the Alzheimer's Disease
- Gradual Disturbances of the Amplitude of Low-Frequency Fluctuations (ALFF) and Fractional ALFF in Alzheimer Spectrum