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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Alzheimer's disease (AD), the most common form of dementia worldwide, is a mixed proteinopathy (β-amyloid, tau and other proteins).
Why it matters
Alzheimer's disease is a heterogeneous disorder with several subtypes defined by the regional pattern of tau pathology and brain atrophy, each with distinct clinical features, age, sex distribution, and biomarker levels. These subtypes include typical, limbic predominant, hippocampal sparing, and minimal atrophy, plus other clinical variants.
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We review the implications of the recently approved aducanumab amyloid-β immunotherapy for treating Alzheimer disease with comorbid cerebral amyloid angiopathy.
Why it matters
This review notes that in clinical trials, amyloid-β immunotherapy has been associated with a high rate of amyloid-related imaging abnormalities, potentially driven by coexisting cerebral amyloid angiopathy. It suggests that coexisting cerebrovascular pathology may modify immunotherapy's efficacy in patients.
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Brain atrophy occurs in aging even in the absence of dementia, but it is unclear to what extent this is due to undetected preclinical Alzheimer disease.
Why it matters
In a cross-sectional group aged 18 to 88 who were free of preclinical Alzheimer disease by amyloid PET and three years of follow-up, age-related atrophy occurred in nearly all brain regions, with different patterns across the temporal, subcortical and frontal areas. This describes normal aging effects and does not treat, cure or prevent Alzheimer's disease.
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Microglia are active modulators of Alzheimer's disease but their role in relation to amyloid plaques and synaptic changes due to rising amyloid beta is unclear.
Why it matters
This study used knock-in mice expressing humanised amyloid beta with familial Alzheimer's disease mutations to examine synaptic transmission, plaques, and microglial roles. It is animal research and does not report a treatment, cure, or prevention for Alzheimer's disease in people.
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Brain iron accumulation has been found to accelerate disease progression in amyloid-β(Aβ) positive Alzheimer patients, though the mechanism is still unknown.
Why it matters
Using human Alzheimer brains, this study identified a subset of microglia with increased iron accumulation and found that iron loading is a prominent feature of activated microglia. This is a histological study of human tissue and does not report a treatment, cure, or prevention.
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We selected 57 patients with LBD (dementia with Lewy bodies [DLB], n = 38; Parkinson disease dementia [PDD], n = 19) with available AD CSF biomarkers and neuropsychological data.
Why it matters
In this group of 57 patients with Lewy body dementia, those who also had likely Alzheimer-type copathology were more impaired on a naming test than those without it. This suggests that Alzheimer-type changes can add to the cognitive problems of people with Lewy body dementia, but it does not test any treatment.
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We examined 54 volunteers (mean age 70.0 years, 56% women, 51% APOE ɛ4 carriers) with the translocator protein (TSPO) tracer [ 11 C]PBR28 to assess neuroinflammation and with [ 11 C] Pittsburgh compound B (PiB) to assess cerebral Aβ accumulation. [ 11 C]PBR28 and [ 11 C]PiB standardized uptake value ratios (SUVRs) were quantified in 6 regions of interests by using the cerebellar cortex as a pseudo-reference and reference region, respectively.
Why it matters
In 54 elderly people without dementia, this study examined whether early amyloid accumulation and metabolic risk factors were associated with neuroinflammation measured by a TSPO tracer. It is an observational imaging study and does not test any treatment for Alzheimer's disease.
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The mean subject score of the ADCRP was significantly higher in the A+T+ group compared to each of the other group (all p p > 0.1).
Why it matters
In 269 patients with mild cognitive impairment, a brain scan pattern called ADCRP predicted conversion to dementia among those with biological Alzheimer's disease (A+T+). It is proposed as a marker of neurodegeneration for estimating risk and time to conversion, not as a treatment.
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Our study shows that ICERS of PFA combined with MI and MI alone amounted to €21,443 and €21,543 respectively per improved Z score point compared to the placebo and are below the WTP of €50,000 while the ICER of PFA alone amounted to €111,720 per improved Z score point.
Why it matters
This cost-effectiveness analysis of the MAPT prevention trial found that a multidomain intervention alone and combined with omega-3 fell below the willingness-to-pay threshold, while omega-3 alone did not. It addresses the economics of prevention strategies, not whether any strategy cures Alzheimer's disease.
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For years, it has been reported that Alzheimer's disease (AD) is the most common cause of dementia.
Why it matters
This review proposes that disturbances in the microbiota-gut-brain axis contribute to Alzheimer's disease through gut barrier changes, immune activation, blood-brain barrier impairment and neuroinflammation. It is a proposed mechanism, not a proven treatment or prevention.
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Genome-wide association studies have led to numerous genetic loci associated with Alzheimer's disease (AD).
Why it matters
Using whole-genome sequencing in families with multiple Alzheimer's cases, this study identified 13 new candidate genes, many related to synaptic function. These are genetic associations that may guide future research, not a treatment or cure.
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Alzheimer's disease (AD) is the most prevalent form of late-onset dementia.
Why it matters
This paper notes that there are currently no approved therapies that can halt or reverse the clinical progression of Alzheimer's disease and discusses the role of microglia and the Nlrp3 inflammasome. It reports no treatment, cure or prevention for the disease.
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Drug repositioning and repurposing can enhance traditional drug development efforts and could accelerate the identification of new treatments for individuals with Alzheimer disease (AD) dementia and mild cognitive impairment.
Why it matters
Drug repositioning and repurposing could speed up the identification of new treatments for people with Alzheimer's disease dementia and mild cognitive impairment. Transcriptional profiling is described as a new and highly efficient way to find candidate drugs, though future work is still needed to use early-stage disease signatures as probes.
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Alzheimer's disease (AD) is pathologically defined by extracellular accumulation of amyloid-β (Aβ) peptides generated by the cleavage of amyloid precursor protein (APP), strings of hyperphosphorylated Tau proteins accumulating inside neurons known as neurofibrillary tangles (NFTs) and neuronal loss.
Why it matters
This review describes how amyloid-beta and hyperphosphorylated tau spread in Alzheimer's disease and notes that no effective treatment is currently available to cure the disease. It summarizes existing knowledge about disease mechanisms rather than reporting a new treatment or prevention.
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Clinical trials focusing on therapeutic candidates that modify β-amyloid (Aβ) have repeatedly failed to treat Alzheimer's disease (AD), suggesting that Aβ may not be the optimal target for treating AD.
Why it matters
This analysis found that elevated β-amyloid and tau better predicted early dementia status while glucose hypometabolism better predicted later dementia status, suggesting treatments may need to be stage-oriented. It proposes targets for future treatment research but does not itself test any treatment, cure, or prevention for Alzheimer's disease.
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Growing evidence indicates an association between cerebral microhemorrhages (MHs) and amyloid β accumulation in Alzheimer disease (AD), but to the knowledge of the authors the association with tau burden is unknown.
Why it matters
This study looked at whether small bleeds in the brain, seen on MRI, are related to tau and amyloid buildup seen on PET scans in people across the Alzheimer's spectrum. It is an observational study and does not test any treatment or prevention.
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Alzheimer's disease (AD) is a devastating neurodegenerative disorder and a leading cause of dementia, with accumulation of amyloid-beta (Aβ) and neurofibrillary tangles (NFTs) as defining pathological features.
Why it matters
This review discusses HMGB1, RAGE and TLR4 as risk factors and possible therapeutic targets in Alzheimer's disease, noting that neuroinflammation links amyloid deposition, tau pathology and neurodegeneration. It states there is no cure to date and offers no confirmed treatment, cure or prevention.
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EEG connectivity analysis via a combination of source/connectivity biomarkers, highly correlating with neuropsychological AD diagnosis, could represent a promising tool in identification of AD patients.
Why it matters
This study used a machine learning classifier on EEG connectivity parameters to distinguish healthy volunteers from people with Alzheimer's disease, reporting very high classification accuracy. The authors suggest this could add a low-cost, easily accessible, non-invasive technique alongside neuropsychological tests.
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There is limited data on cerebrospinal fluid (CSF) biomarkers in sporadic amyloid-β (Aβ) cerebral amyloid angiopathy (CAA).
Why it matters
This study compared cerebrospinal fluid markers in 10 patients with cerebral amyloid angiopathy, 20 with Alzheimer's disease, and 10 controls. It is a small study describing biomarker profiles and does not show a treatment or cure.
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The unbiased amyloid, tau, and neurodegeneration (A/T/N) classification is designed to characterize individuals in the Alzheimer continuum and is currently little explored in clinical cohorts.
Why it matters
This study retrospectively applied the amyloid, tau, and neurodegeneration (A/T/N) classification to a clinical cohort with long-term follow-up. It compares a classification system with clinical outcomes, not a treatment, cure, or prevention for Alzheimer's disease.
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48/100
In 2014 and 2016, the overall prevalence of AD/ADRD diagnoses was 5.6% and 6.5%, respectively.
Why it matters
This study found that the diagnosed prevalence of Alzheimer's disease and related dementias in Medicare Advantage plans was 5.6% in 2014 and 6.5% in 2016, lower than rates reported in Medicare fee-for-service. By one year after the index date, 32% of beneficiaries with dementia had disenrolled from their plan.
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Amyloid imaging with PET and measuring cortical thickness with MRI are suitable biomarkers to detect disease progression in early AD within a small sample.
Why it matters
This study compared three imaging markers over 24 months in early Alzheimer's disease and found that amyloid PET and cortical thickness needed far fewer participants than FDG-PET to detect change. It is about choosing markers for trials and does not test any treatment, cure, or prevention.
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On the basis of the independent validation dataset, the 18 F-FDG PET model yielded a significantly higher predictive value than the amyloid PET model.
Why it matters
For predicting conversion from mild cognitive impairment to Alzheimer dementia, an 18F-FDG PET model performed significantly better than an amyloid PET model, but both were inferior to a model using nonimaging variables alone and both improved when nonimaging variables were added. The best accuracy came from combining 18F-FDG PET, amyloid PET, and nonimaging variables, which allowed stratification of patients into low-, medium-, and high-risk groups with 5-year free-of-conversion rates of 100%, 64%, and 24%.
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The Alzheimer's disease (AD) afflicted brain is neuropathologically defined by extracellular amyloid-β (Aβ) plaques and intraneuronal neurofibrillary tangles composed of hyperphosphorylated tau protein.
Why it matters
This review summarizes evidence that the protein alpha-synuclein is involved in the pathophysiology of Alzheimer's disease and that higher cerebrospinal fluid alpha-synuclein levels have been linked to cognitive decline. It is a review of mechanisms and biomarkers, not a treatment or prevention trial.
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48/100
In MCI reverters, abnormal biomarkers for AD pathology are associated with subsequent decline.
Why it matters
Among 61 people with mild cognitive impairment who reverted to normal cognition, those who later declined were older and had higher amyloid PET burden and higher CSF tau levels. This is about using biomarkers to predict outcome after reversion, not about treating, curing or preventing Alzheimer's disease.
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.
- ADAM10 y su implicación en la enfermedad de Alzheimer
- Preparation of a recombinant cDNA library from poly(A+) RNA of the Alzheimer brain. Identification and characterization of a cDNA copy encoding a glial-specific protein
- Comprehensive Review on Alzheimer Disease: Causes, Risk Factors, Pathology, Mechanisms
- Prevalence of Diagnosed Alzheimer’s Disease and Related Dementias in Medicare Advantage
- Shifting paradigms: The central role of microglia in Alzheimer's disease
- The genetic landscape of Parkinson's disease
- MRI Characterizes the Progressive Course of AD and Predicts Conversion to Alzheimer's Dementia 24 Months Before Probable Diagnosis
- Odor identification deficit predicts clinical conversion from mild cognitive impairment to dementia due to Alzheimer's disease
- The impact of cholinesterase inhibitors on cognitive trajectories in mild cognitive impairment patients based on amyloid beta status
- [Oxidative stress hypothesis for Alzheimer's disease and its potential therapeutic implications]