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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We extend prior work using BAG from sporadic AD to ADAD, noting consistent results.
Why it matters
In people with autosomal dominant Alzheimer's disease mutations, brain-predicted age was advanced about 7 years before expected symptom onset and was strongly associated with pTau-181. This supports brain age as a marker of early disease progression, not a treatment or cure.
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Lecanemab is a humanized monoclonal antibody that is selective for soluble amyloid-beta (Aβ) aggregates.
Why it matters
In the Clarity AD phase III trial, lecanemab reduced brain amyloid levels and showed moderate improvement in clinical measures of cognition and function compared with placebo at 18 months. It reduces cognitive decline but raises concerns about intravenous administration, cost, and magnetic resonance imaging needs.
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Geographical disparities in mortality among Alzheimer`s disease (AD) patients have been reported and complex sociodemographic and environmental determinants of health (SEDH) may be contributing to this variation.
Why it matters
This cross-sectional study used machine learning to link county-level social and environmental factors to all-cause mortality among older people with Alzheimer's disease. It identifies factors associated with mortality and does not test any treatment or cure.
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Alzheimer's disease (AD), characterized by the β-amyloid protein (Aβ) deposition and tau hyperphosphorylation, is the most common dementia with uncertain etiology.
Why it matters
This paper discusses the hypothesis that dysregulated metal ions such as iron, copper and zinc are associated with amyloid deposition, tau hyperphosphorylation, neuronal loss and neuroinflammation in Alzheimer's disease. It also considers metal chelators for their anti-neuroinflammatory effect, but this is a discussion of a hypothesis rather than evidence that chelators treat or prevent the disease.
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Alzheimer's disease (AD), the most common form of dementia, has increasing incidence, increasing mortality rates, and poses a huge burden on healthcare.
Why it matters
This review notes that no currently approved Alzheimer's drugs influence disease progression and that many trials targeting amyloid plaques or tangles failed or gave inconclusive results. It points to oxidative stress, mitochondrial dysfunction, and neuroinflammation as possible new targets, but most promising molecules have only been tested in vitro or in animal models and need much more research before clinical use.
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We aimed to elucidate the dynamics of blood biomarkers according to the severity of cognitive impairment in patients with type 2 diabetes mellitus (DM) and to identify useful biomarkers for diabetes-related dementia.
Why it matters
This study compared blood markers, including soluble TREM2, in people with and without type 2 diabetes across different levels of cognitive function. It found significantly lower levels of serum sTREM2 in all cognitive strata, but it is a cross-sectional study and does not show whether this marker can be used to treat or prevent dementia.
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The study included 2,284,175 FFS Medicare beneficiaries with an ADRD diagnosis in 2017.
Why it matters
This study found that African American and Hispanic beneficiaries with Alzheimer's disease and related dementias were more likely than White beneficiaries to switch from fee-for-service to Medicare Advantage. It does not test any treatment, cure, or prevention, and it underscores the need to monitor quality and equity of access and care for these populations.
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Alzheimer disease (AD) is a leading cause of dementia that has gained prominence in our aging society.
Why it matters
Blood protein models using mass spectrometry classified Alzheimer disease with about 85% accuracy and monitored progression with about 79% accuracy, doing better than APOE genotype alone or a cognitive score. This is a screening approach and does not treat, cure or prevent the disease.
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White matter structural connectivity was lower in autosomal dominant Alzheimer disease mutation carriers compared with noncarriers and correlated with estimated years to symptom onset.
Why it matters
In this cross-sectional study of people with autosomal dominant Alzheimer disease mutations, carriers had lower structural connectivity in one brain network than noncarriers, and this correlated with estimated years to symptom onset. No significant relationship was found between global cortical amyloid burden and estimated years to symptom onset.
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Forty-one participants (30 male, 11 female) with a mean (SD) age at death of 75.7 (10.6) years were included.
Why it matters
In 41 autopsied participants, cerebral amyloid angiopathy burden was not associated with PiB-PET signal, while amyloid plaques were associated in all regions. This is a pathology-imaging correlation study and does not test any treatment, cure, or prevention for Alzheimer's disease.
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Clinicians reported high diagnostic confidence in 83% of 18 F-FDG PET compared to 67% for CBF-SPECT (P = 0.001).
Why it matters
In patients referred for cognitive impairment assessment, 18F-FDG PET was better than CBF-SPECT at detecting Alzheimer's disease confirmed by amyloid PET. This is about improving diagnosis, not about treating, curing or preventing the disease.
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Amyloid-beta (Aβ) 42/40 ratio, tau phosphorylated at threonine-181 (p-tau), and total-tau (t-tau) are considered core biomarkers for the diagnosis of Alzheimer's disease (AD).
Why it matters
This study used an unsupervised machine learning clustering algorithm on cerebrospinal fluid biomarker data from two large patient cohorts. It found patients could be classified into six clusters by biomarker profile, which may help with diagnosis but does not treat or prevent Alzheimer's disease.
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Gut microbiota can influence human brain function and behavior.
Why it matters
This study analysed fecal samples from 60 Alzheimer's disease patients and 32 healthy controls to look at gut microbiota composition and its link to cognitive and neuropsychiatric symptoms. It reports associations only and does not test any treatment, cure or prevention.
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45/100
Alzheimer's disease (AD) is the most common form of neurodegenerative dementia and its timely diagnosis remains a major challenge in biomarker discovery.
Why it matters
Using automated machine learning on publicly available blood-based omics datasets, this study produced three diagnostic biosignatures for Alzheimer's disease with AUCs ranging from 0.846 to 0.975. These results offer options for minimally invasive blood-based diagnostic tests, but the authors note they await clinical validation based on respective laboratory assays.
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The trajectories of depression and apathy (measured with the Neuropsychiatric Inventory or its questionnaire) were separately modeled using growth mixture models for two cohorts (National Alzheimer's Coordinating Center, NACC, n = 22 760 and Alzheimer's Disease Neuroimaging Initiative, ADNI, n = 1 733).
Why it matters
This study examined how depression and apathy change over five years in people with normal thinking, mild cognitive impairment, or Alzheimer's dementia, and whether Alzheimer's biomarkers predict those changes. Understanding these links could help identify and manage mood symptoms in people with or at risk of Alzheimer's.
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Parkinson's disease (PD) research is beginning to focus on early disease modification and prevention.
Why it matters
This review notes that large trials aiming to slow or prevent Alzheimer's dementia by targeting amyloid-beta aggregation did not produce detectable clinical effects. It draws lessons for Parkinson's disease research and does not offer a treatment, cure, or prevention for Alzheimer's disease.
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Dysregulation of insulin signaling pathway with reduced downstream neuronal survival and plasticity mechanisms is a fundamental abnormality observed in Alzheimer's disease (AD) brain.
Why it matters
In post-mortem brain samples, people with Down syndrome showed markers of brain insulin resistance early in life, before Alzheimer's disease pathology developed. This is an observational study of brain tissue and does not show that treating insulin resistance prevents or cures Alzheimer's disease.
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These findings suggest that NfL can be used to monitor cognitive decline in aging and Alzheimer's disease and that an attentional control composite may be a better outcome for tracking general neurodegenerative effects on cognition.
Why it matters
In 255 cognitively healthy adults, NfL predicted decline in attention and global cognition but not memory, independent of amyloid status. The study only examines how biomarkers relate to cognitive decline and does not test any treatment, cure, or prevention.
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275 cognitively normal controls (NC), 100 subjective memory complaint (SMC), 559 mild cognitive impairment (MCI) and 143 Alzheimer's disease dementia subjects from the Alzheimer's Disease Neuroimaging Initiative received ( 18 F)-florbetapir positron emission tomography (PET) scans.
Why it matters
This study examined the relationship between amyloid burden on PET scans and the frequency and incidence of neuropsychiatric symptoms in 275 cognitively normal controls, 100 with subjective memory complaints, 559 with mild cognitive impairment, and 143 with Alzheimer's disease dementia. Yearly assessments tracked these symptoms to see if amyloid levels were linked to their occurrence.
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18 F-PI-2620 showed peak brain uptake around 5 min after injection and fast washout from nontarget regions.
Why it matters
This first-in-humans study found that the tau PET tracer 18F-PI-2620 was safe and well tolerated and showed higher uptake in brain regions of people with Alzheimer disease than in healthy controls. It is an early imaging study of a tracer for detecting tau, not a test of any treatment, cure, or prevention.
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Individuals with intact cognition and neuropathology consistent with Alzheimer's disease (AD) are referred to as asymptomatic AD (AsymAD).
Why it matters
Comparing brain tissue from people with asymptomatic Alzheimer's pathology, symptomatic Alzheimer's and controls, this study found increased transcriptomic activity in the frontal cortex of asymptomatic cases and disturbances in energy pathways in both groups. It points to possible early biological changes and potential targets, but it is tissue analysis and does not test any treatment.
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Alzheimer's disease (AD) is a neurodegenerative disease characterized by progressive memory loss and dementia.
Why it matters
This review notes that inflammation is involved in Alzheimer's disease and that epidemiological studies suggested anti-inflammatory drugs might reduce incidence, but clinical trials with these drugs have not been successful. It reports no effective anti-inflammatory treatment for Alzheimer's disease.
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Alzheimer's disease (AD) genetics implies a causal role for innate immune genes, TREM2 and CD33, products that oppose each other in the downstream Syk tyrosine kinase pathway, activating microglial phagocytosis of amyloid (Aβ).
Why it matters
In APPsw transgenic mice, low-dose curcumin shifted innate immune gene expression in a direction predicted to lower Alzheimer's risk. These are animal findings, so it is not yet known whether curcumin has the same effect or benefit in people.
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The National Institute on Aging and Alzheimer's Association (NIA-AA) have proposed a new Research Framework: Towards a biological definition of Alzheimer's disease, which uses a three-biomarker construct: Aß-amyloid, tau and neurodegeneration AT(N), to generate a biomarker based definition of Alzheimer's disease.
Why it matters
This study grouped participants in the AIBL study using the NIA-AA research framework, which classifies people by amyloid, tau and neurodegeneration biomarkers, and compared their clinical and cognitive profiles. It is about a biological definition and classification of Alzheimer disease, not about treating or preventing it.
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The Alzheimer's Disease Sequencing Project (ADSP) undertook whole exome sequencing in 5,740 late-onset Alzheimer disease (AD) cases and 5,096 cognitively normal controls primarily of European ancestry (EA), among whom 218 cases and 177 controls were Caribbean Hispanic (CH).
Why it matters
This large genetic study identified new and predicted functional variants in genes already associated with Alzheimer disease, including genes involved in immune response and transcriptional regulation. It adds to understanding of genetic risk but does not provide a treatment, cure, or prevention.
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.
- Meta-analysis for genome-wide association study identifies multiple variants at the BIN1 locus associated with late-onset Alzheimer's disease
- Clinical and multimodal biomarker correlates of ADNI neuropathological findings
- Cerebral atrophy in Parkinson's disease with and without dementia: a comparison with Alzheimer's disease, dementia with Lewy bodies and controls
- Longitudinal assessment of Aβ and cognition in aging and Alzheimer disease
- Age, vascular health, and Alzheimer disease biomarkers in an elderly sample
- Fine mapping of the chromosome 12 late-onset Alzheimer disease locus: potential genetic and phenotypic heterogeneity
- Alzheimer's disease associated with Down syndrome: a genetic form of dementia
- Age-sex differences in Alzheimer’s and related dementias burden and risk factors in east and Southeast Asia: results from the 2021 GBD study
- Genetic linkage studies suggest that Alzheimer's disease is not a single homogeneous disorder
- Downstream Biomarker Effects of Gantenerumab or Solanezumab in Dominantly Inherited Alzheimer Disease: The DIAN-TU-001 Randomized Clinical Trial