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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54/100
The genetic variants play a crucial role in the pathogenesis of Alzheimer's disease (AD), while the relationships of specific single nucleotide polymorphisms (SNPs) with AD are still controversial.
Why it matters
Pooling 35 case-control studies covering 15 genetic variants, this meta-analysis found that variants in PICALM and SORL1 were linked to Alzheimer's risk, while the GAB2 variant rs2373115 was not. The T allele of PICALM rs3851179 was associated with a 13 % increase in risk, and seven SORL1 variants were tied to either higher or lower risk. These are risk associations, so they help map who may be more susceptible rather than point directly to a treatment.
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We replicated the CLU-MS4A4E interaction in a large case-control series and observed APOE ε4 and possible dominant effect.
Why it matters
Using 3837 cases and 4145 controls, this study confirmed that variants in the CLU and MS4A4E genes interact to raise Alzheimer's risk, especially in people without APOE ε4. The authors estimate an 8% decrease in Alzheimer's incidence without these risk alleles and identify possible causal variants. This is a statistical genetic estimate, pointing to gene combinations worth further study.
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Treatment outcomes in CitAD showed modest, although statistically significant, influence of genetic variation at HTR2A and HTR2C loci.
Why it matters
Using data from a 9-week trial in which citalopram improved agitation and caregiver distress, this analysis looked at whether six genetic variants affected how well people responded. It found significant interactions for two serotonin-related genes, but the influence of these genes on treatment outcomes was modest.
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Alzheimer's disease (AD) can present with distinct clinical variants.
Why it matters
Using voxel-based morphometry, this study mapped brain atrophy patterns in early clinical stages of four Alzheimer's disease phenotypes, including posterior cortical atrophy and logopenic variant primary progressive aphasia. It aims to aid early diagnosis and understanding of disease progression, not treatment, cure or prevention.
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The Alzheimer's Disease Neuroimaging Initiative (ADNI), launched in 2004, has worked to accelerate drug development by validating imaging and blood/cerebrospinal fluid biomarkers for Alzheimer's disease clinical treatment trials.
Why it matters
This is an update on the Alzheimer's Disease Neuroimaging Initiative (ADNI), a large project that shares brain scan and fluid biomarker data to help drug development. It is about research infrastructure and does not itself test a treatment, cure, or prevention.
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Despite significant progress, a disease-modifying therapy for Alzheimer's disease (AD) has not yet been developed.
Why it matters
This was a Phase Ib trial testing the drug saracatinib, which targets the Fyn kinase pathway linked to amyloid beta toxicity, to see whether it is safe and reaches the brain. It is an early-stage safety study, so it does not show whether the drug actually helps or prevents Alzheimer's disease.
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This report discusses the public health impact of Alzheimer’s disease (AD), including incidence and prevalence, mortality rates, costs of care and the overall effect on caregivers and society.
Why it matters
This report covers the public health impact of Alzheimer's disease, including incidence, prevalence, mortality, costs of care and effects on caregivers. It contains no findings on treating, curing or preventing the disease.
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With the aging of the population, the burden of Alzheimer's disease (AD) is rapidly expanding.
Why it matters
This 2014 review (not a new study) notes that women are "disproportionally affected" by Alzheimer's, while men "may have a higher risk" of mild cognitive impairment. It offers one possible reason, that men may die of other causes earlier so "only the most resilient men" reach older ages, and stresses that "many other factors" also need to be considered. It separates sex (biology, such as chromosomes and hormones) from gender (social factors, such as access to education and occupation) and argues both must be understood to design prevention and treatment. It does not test any intervention.
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The global prevalence of dementia is as high as 24 million, and has been predicted to quadruple by the year 2050.
Why it matters
This review describes how common Alzheimer's disease is, its costs, and its hallmark brain changes of amyloid plaques and neurofibrillary tangles. It states that the underlying causes remain unclear but are probably due to both environmental and genetic factors, and it discusses biomarkers that may be used for risk assessment and diagnosis.
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Using quantitative polymerase chain reaction techniques, we measured circulating cell-free mitochondrial DNA (mtDNA) in cerebrospinal fluid (CSF) from study participants, selected from a cohort of 282 subjects, who were classified according to their concentrations of amyloid β1-42, total tau, and phosphorylated tau and by the presence or absence of dementia, into asymptomatic subjects at risk of AD, symptomatic patients diagnosed with sporadic AD, presymptomatic subjects carrying pathogenic PSEN1 mutations, and patients diagnosed with frontotemporal lobar degeneration (FTLD).
Why it matters
This study measured cell-free mitochondrial DNA in cerebrospinal fluid and found low concentrations in people at risk of Alzheimer's disease before symptoms appeared, including presymptomatic carriers of PSEN1 mutations. It identifies a possible early biochemical marker, not a treatment, cure or prevention.
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Dementia is increasingly being recognized in cases of Parkinson's disease (PD); such cases are termed PD dementia (PDD).
Why it matters
This review describes how the spread of alpha-synuclein pathology relates to dementia in Parkinson's disease, and notes that up to 50% of patients with Parkinson's disease dementia also develop amyloid-beta plaques and tau tangles sufficient for a secondary Alzheimer's disease diagnosis. It states that understanding these relationships is crucial for developing effective disease-modifying treatments, but reports no treatment or cure.
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Alzheimer's Disease (AD) currently affects more than 5 million Americans, with numbers expected to grow dramatically as the population ages.
Why it matters
This metabolomics study found many altered metabolites and pathways in plasma and cerebrospinal fluid of people with MCI compared with cognitively normal individuals, with the number of affected pathways increasing with disease severity. These findings may help identify early disease mechanisms and therapeutic targets, but no treatment was tested.
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The HCRU and costs were greater for AD members during the year prior to diagnosis and during postdiagnosis years 1 and 2 compared to controls.
Why it matters
This study found that Medicare Advantage members newly diagnosed with Alzheimer's disease had greater health care utilization, costs, and comorbidity burden compared to matched controls without Alzheimer's disease. The higher utilization and costs were seen both before and after diagnosis.
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Ventricular volume trajectory is more sensitive than total brain and hippocampal volume trajectories as a marker of accruing Alzheimer disease and vascular pathology in elderly individuals.
Why it matters
This autopsy study found that brain shrinkage over time was linked to several factors including infarcts, tangles, plaques, APOE ε4, and dementia diagnosis. The authors note there may be other factors not measured in this study contributing to brain atrophy.
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None of the lifestyle variables were correlated with the biomarkers, and the path associations between lifestyle variables and biomarkers were not significant (p > 0.05).
Why it matters
In 515 nondemented older adults, intellectual and physical activity were not associated with amyloid, FDG-PET, or hippocampal volume biomarkers, though intellectual activity was linked to cognitive performance. This is a null result for lifestyle activity and Alzheimer's disease biomarkers, not evidence of prevention.
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Plasma biomarker results confirm cerebrospinal fluid studies reporting increased levels of pancreatic polypeptide and N-terminal protein B-type brain natriuretic peptide in patients with AD and mild cognitive impairment.
Why it matters
In this cohort, several plasma proteins differed between people with Alzheimer's disease or mild cognitive impairment and controls, and the APOE genotype was linked to a distinct biochemical profile. These findings are about blood-based screening and do not show a treatment, cure, or prevention.
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Anxiety, apathy and depression are common in subjects with mild cognitive impairment (MCI) and may herald Alzheimer's disease (AD).
Why it matters
This study investigated whether anxiety, apathy, and depression in people with mild cognitive impairment correlate with cerebrospinal fluid markers for Alzheimer disease. It is an observational study and does not test any treatment, cure, or prevention.
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Two thousand three hundred and thirty two nonselected brains from 1- to 100-year-old individuals were examined using immunocytochemistry (AT8) and Gallyas silver staining for abnormal tau; immunocytochemistry (4G8) and Campbell-Switzer staining were used for the detection ofβ-amyloid.
Why it matters
Examined brains from people aged 1 to 100 years for abnormal tau and amyloid plaques. Tau changes appeared in the brainstem before the first plaques, and 44.2% of cases had plaques. The authors suggest tau changes tied to sporadic Alzheimer's may begin earlier than previously thought, possibly in the lower brainstem.
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A liability threshold model of disease was used to estimate heritability of EOAD and late-onset Alzheimer disease (AD) using concordance for AD among parent-offspring pairs.
Why it matters
Using a liability threshold model in 5,370 people with probable Alzheimer's disease and parental history, this study estimated heritability and found autosomal recessive causes likely in early-onset cases. It is about inheritance patterns and offers no treatment, cure or prevention.
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A total of 401 elderly participants in the Alzheimer's Disease Neuroimaging Initiative who were cognitively normal, who had mild cognitive impairment, or who had AD dementia.
Why it matters
In 401 older adults from the Alzheimer's Disease Neuroimaging Initiative, some cognitively normal, some with mild cognitive impairment and some with Alzheimer's dementia, this study compared how often three markers were abnormal at each stage: amyloid-β42 and total tau in spinal fluid, and hippocampal size on brain scans. The normal-versus-abnormal cut-offs were set using separate autopsy samples. The aim was to test whether these markers "depart from normality in a temporally ordered manner". The study is about the order in which markers change, not about treating, curing or preventing Alzheimer's.
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When compared with the other groups, AD patients demonstrated significantly higher SUVRs (P Conclusion (18)F-florbetaben had high sensitivity for AD, clearly distinguished patients with FTLD from AD, and provided results comparable to those reported with (11)C-Pittsburgh Compound B in a variety of neurodegenerative diseases.
Why it matters
This study found that amyloid imaging with (18)F-florbetaben showed high sensitivity for Alzheimer disease and clearly distinguished patients with frontotemporal lobar degeneration from those with Alzheimer disease. It provided results comparable to those reported with (11)C-Pittsburgh Compound B in a variety of neurodegenerative diseases.
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It introduces criteria to determine whether an image is associated with an intermediate-to-high likelihood of pathologic AD or with having any identifiable cortical amyloid level above that seen in low-risk young controls.
Why it matters
Across several imaging centres, florbetapir PET amyloid readings (SUVR) averaged 1.39 in 68 people with probable Alzheimer disease, 1.17 in 60 with mild cognitive impairment and 1.05 in 82 healthy adults aged 55 or older; the groups differed significantly. The study proposed two cut-offs: 1.17 or above for amyloid at levels associated with Alzheimer pathology (set from scans and autopsies of 19 end-of-life patients), and above 1.08 for any amyloid beyond that seen in young, low-risk adults (set from 46 people aged 18–40 without APOE ε4). These are group averages from one time point: the summary as held gives no accuracy figures or follow-up, so a single reading is not a diagnosis.
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One third of patients with pathologic confirmed EOAD presented with atypical symptoms.
Why it matters
In pathologically confirmed early-onset Alzheimer's disease, atypical presentations were common and often led to incorrect initial diagnoses, while APOE genotype did not differ significantly between typical and atypical presentations. APOE ε4 was more frequent in those with a family history of Alzheimer's disease.
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We conclude that FHm individuals without dementia have progressive gray matter volume reductions in select AD-vulnerable brain regions, specifically the precuneus and parahippocampal gyrus.
Why it matters
In this small longitudinal imaging study, cognitively normal people whose mothers had Alzheimer disease showed greater brain atrophy over two years than those without a parental history. It describes a risk pattern and does not test any treatment or prevention.
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The global prevalence of dementia is estimated to be as high as 24 million, and is predicted to double every 20 years through to 2040, leading to a costly burden of disease.
Why it matters
A 2011 narrative review, not a new study, that gives an overview of how Alzheimer's is diagnosed, how common it is, its risk factors and possible biomarkers. It quotes an estimate that dementia affects "as high as 24 million" people worldwide, a number "predicted to double every 20 years through to 2040", and describes plaques and tangles as the disease's brain hallmarks, while stating that their underlying causes "remain unclear". It reports no new data and tests no treatment; the specific criteria, risk factors and biomarkers it reviews are not given in this record.
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.
- Amyloid-beta(1-42), total tau, and phosphorylated tau as cerebrospinal fluid biomarkers for the diagnosis of Alzheimer disease
- Blood-based biomarkers of Alzheimer’s disease and incident dementia in the community
- Sequence of Alzheimer disease biomarker changes in cognitively normal adults: A cross-sectional study
- Intermittent Fasting Ameliorates β‐Amyloid Deposition and Cognitive Impairment Accompanied by Decreased Lipid Droplet Aggregation Within Microglia in an Alzheimer's Disease Model
- The genetics of Alzheimer's disease
- Artificial intelligence in neurodegenerative diseases research: a bibliometric analysis since 2000
- Genome-wide association study implicates a chromosome 12 risk locus for late-onset Alzheimer disease
- Cerebrospinal fluid protein biomarkers for Alzheimer's disease
- Beta-amyloid, neuronal death and Alzheimer's disease
- Value-based prices of emerging disease-modifying therapies for Alzheimer's disease in 174 countries: a cost-effectiveness and threshold analysis