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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Among 558 amnestic MCI participants (168 ChEI users), ChEI users exhibited higher risk of progression to AD dementia (hazard ratio = 1.77, 95% confidence interval: 1.15 to 2.73, p = 0.001).
Why it matters
In this longitudinal study of 558 people with amnestic MCI, those taking cholinesterase inhibitors had a higher risk of progressing to Alzheimer's dementia and continued to decline cognitively after starting treatment. The findings suggest that cholinesterase inhibitor use in MCI was associated with accelerated progression, independent of amyloid-beta status, and raise questions about optimal timing of treatment.
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Data from 17 107 individuals (321 Asian, 635 Black, 829 Hispanic, and 15 322 White) with MCI or dementia and amyloid PET were analyzed between April 2020 and January 2022.
Why it matters
Among people with MCI or dementia, Asian, Black, and Hispanic participants had lower odds of a positive amyloid PET scan than White participants in adjusted analyses. The authors suggest these differences may indicate different underlying causes of cognitive impairment and could guide future treatment and prevention approaches.
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< 0.001). Shape features demonstrated the highest predictive accuracy for conversion, with areas under the curve of 0.891 at baseline and 0.898 at 2 years.
Why it matters
This longitudinal ADNI study found that combining amyloid PET and MRI biomarkers, particularly shape features, predicted conversion from MCI to Alzheimer's disease with areas under the curve of 0.891 at baseline and 0.898 at 2 years. The findings support combined imaging for early diagnosis and targeted interventions, but the study itself does not test any treatment.
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Plasma phosphorylated threonine 181 of tau (pTau181) and amyloid beta (Aβ) are biomarkers for differential diagnosis and preclinical detection of Alzheimer disease (AD).
Why it matters
In 2086 people of African American, Caribbean Hispanic, and Peruvian ancestry, plasma pTau181 was associated with Alzheimer's disease and was consistent across cohorts, though predictive value varied. This is a biomarker generalizability study and does not test any treatment, cure, or prevention.
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The FCAAS-4 achieved a mean area under the receiver operating characteristic curve (AUC-ROC) of 0.74 (95% confidence interval: 0.71-0.77) and a Harrell generalized c-index of 0.72 (0.70-0.75).
Why it matters
A web tool, the Florey CAA Score, was developed to predict cerebral amyloid angiopathy severity, which can otherwise only be determined after death, and showed promising performance in the reported models. It is a risk-stratification tool and does not treat, cure or prevent Alzheimer's disease.
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By 2060, ADRD cases in China are projected to reach approximately 49.89 million, with the highest prevalence and economic burden concentrated in provinces such as Shandong, Sichuan, Jiangsu, Henan, and Guangdong.
Why it matters
Projections suggest that by 2060 China could have about 49.89 million ADRD cases, with formal care costs exceeding $1 trillion annually and informal caregiving making up 60% to 80% of total costs. The paper calls for stronger long-term care, caregiver support, and regionally tailored policies, but does not test any treatment, cure, or prevention.
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Detecting Alzheimer's disease (AD) in its earliest stages, particularly during an onset of Mild Cognitive Impairment (MCI), remains challenging due to the overlap of initial symptoms with normal aging processes.
Why it matters
This study used eye movements and speech, analyzed with a fusion neural network, to classify mild cognitive impairment and Alzheimer's disease versus healthy controls in 78 participants. It is a small diagnostic study and does not test any treatment, cure or prevention.
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Alzheimer's disease (AD) is a prevalent neurodegenerative disease characterized by both amnestic and non-amnestic clinical manifestations.
Why it matters
This review notes that several proposed mechanisms for Alzheimer's disease, including amyloid, tau, neuroinflammation, oxidative stress, mitochondrial dysfunction, cholinergic and vascular hypotheses, are not mutually exclusive and all appear to play some role. It does not report any treatment, cure or prevention result, only the need to clarify these mechanisms to develop future interventions.
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Development of validated biomarkers to detect early Alzheimer disease (AD) neuropathology is needed for therapeutic AD trials.
Why it matters
This article describes the clinical significance of cerebrospinal fluid and plasma Alzheimer's disease biomarkers and the move toward blood-based tests for amyloid and tau pathology. It is about developing and using biomarkers for detection, not about treating, curing, or preventing Alzheimer's disease.
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The neurodegenerative disease field has enjoyed extremely limited success in the development of effective therapeutics.
Why it matters
This review argues that a precision medicine approach, which identifies and addresses multiple individual contributors to cognitive decline, may be more effective than single-target treatments, based on recent proof-of-concept trials. The authors state that much larger randomized controlled trials are needed before precision medicine can be established as a standard of care for prevention and treatment.
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Three-hundred seventy nine participants underwent blood draw (71.9 ± 7.8 years old, 60.2% female, 57% Hispanic of which 88% were Cuban or South American) and 240 completed Aβ-PET.
Why it matters
Among 379 Hispanic and non-Hispanic older adults, plasma p-tau181 was higher in those with amnestic mild cognitive impairment and dementia and related to brain amyloid burden. This is an observational biomarker study and does not test any treatment, cure, or prevention for Alzheimer's disease.
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Genome-wide association studies (GWAS) of cerebrospinal fluid (CSF) Alzheimer's Disease (AD) biomarker levels have identified novel genes implicated in disease risk, onset and progression.
Why it matters
This genetic analysis found six genome-wide significant signals for plasma Alzheimer's biomarkers, with APOE associated with several of them, and showed genetic overlap between CSF and plasma biomarkers. It is about understanding the genetics of biomarkers, not about a treatment or cure.
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The database search returned 262 results, and after assessment for eligibility, 21 studies were selected.
Why it matters
This review of 21 studies suggests that tau PET-based Braak staging may help stage Alzheimer's disease and correlates with clinical and biomarker measures. However, definitions of brain regions varied between studies, so standardization is needed before it can be applied in practice.
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Use of pharmacological treatments is one possible modifiable risk factor for cognitive disorders.
Why it matters
This Finnish case-control study found that use of any muscle relaxant was associated with a slightly increased risk of Alzheimer's disease, with stronger association for longer use, though no dose-response was observed and tizanidine was not associated. It identifies a possible modifiable risk factor but does not establish that muscle relaxants cause Alzheimer's disease or that avoiding them prevents it.
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Alzheimer's disease (AD), the most common form of dementia, is characterized by the accumulation of amyloid β (Aβ) and hyperphosphorylated tau protein aggregates.
Why it matters
This review describes the inflammatory response in Alzheimer's disease as having a dual function, potentially protective by increasing amyloid-beta clearance but also contributing to amyloid-beta and tau overproduction and neurodegeneration. It reports no treatment, cure, or prevention.
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Alzheimer's disease (AD) is a neurodegenerative disorder characterized by memory loss and personality changes, eventually leading to dementia.
Why it matters
This review summarizes the advantages and limitations of various mouse models of Alzheimer's disease used to study amyloid and tau pathology. It is a description of research tools, not a treatment, cure or prevention for patients.
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TSPO and x c - overexpression can be assessed by [ 18 F]DPA-714 and [ 18 F]FSPG, respectively, and correlate with the level of Aβ plaque deposition obtained with a PET amyloid tracer.
Why it matters
In 5xFAD mice, PET tracers for TSPO and the xc- system showed increasing uptake over time in several brain regions, correlating with amyloid plaque deposition. This is animal imaging research on biomarkers of neuroinflammation, not a treatment or cure.
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Several recent research studies show high performance of blood biomarkers to identify Alzheimer's disease also in the pre-dementia mild cognitive impairment (MCI) stage, but data from the routine clinical care memory clinic setting are needed.
Why it matters
In 144 memory clinic patients, blood levels of pTau181 and NFL, and the ratios Aβ42/Aβ40 and pTau181/Aβ42, could tell apart people with Alzheimer's dementia, mild cognitive impairment, and subjective cognitive decline. This supports using these blood markers in routine memory clinic settings, not just in research.
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The study of Alzheimer's disease (AD), the most common cause of dementia, faces challenges in terms of understanding the cause, monitoring the pathogenesis, and developing early diagnoses and effective treatments.
Why it matters
This work used graphene-assisted Raman spectroscopy and machine learning to classify Alzheimer's and non-Alzheimer's brain tissue from transgenic mice, reaching 98% accuracy and identifying markers including Aβ and tau. Because it was done in animal brains, it is early-stage and does not yet provide a treatment, cure, or prevention for people.
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Participants had a mean age of 71.3 (SD 4.6) years; 40.6% were male; and 34.6% were APOE ε4 positive.
Why it matters
In 4,484 cognitively unimpaired participants, those in higher Stages of Objective Memory Impairment had higher global amyloid on PET, and a subset with amyloid also showed smaller volumes in memory-related brain regions. This links a memory test to Alzheimer's pathology but does not test any treatment.
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49/100
Aducanumab was granted accelerated approval with a conflicting evidence base, near-unanimous Food and Drug Administration Advisory Committee vote to reject approval, and a widely criticized launch price of $56,000 per year.
Why it matters
This analysis used a Markov model to estimate the cost-effectiveness of aducanumab plus supportive care compared with supportive care alone over a lifetime horizon. It addresses cost and value rather than whether the drug cures or prevents Alzheimer's disease.
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Alzheimer's disease (AD) is a neurodegenerative disorder accounting for over 50% of all dementia patients and representing a leading cause of death worldwide for the global ageing population.
Why it matters
This review discusses oxidative damage as a possible contributor to Alzheimer's disease mechanisms and as a source of peripheral biomarkers. It focuses on oxidative damage products in blood, cerebrospinal fluid, urine and saliva as possible tools for early diagnosis and monitoring, but reports no treatment or cure.
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As a result of the PLST training, there was a decrease in the behavioural problems of Alzheimer's patients, along with a decrease in the care burden of the caregivers and an increase in their care satisfaction.
Why it matters
In this small trial of 29 caregivers, training based on the Progressively Lowered Stress Threshold model was linked to fewer behavioral problems in patients and lower caregiver burden, but only the increase in caregivers' care satisfaction was statistically significant. The small number of participants limits how much these results can be generalized.
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The gFC was reduced in MC compared with NC participants.
Why it matters
In people with autosomal dominant Alzheimer disease, global functional connectivity was reduced compared with non-carriers and changed in a nonlinear way relative to estimated years to symptom onset, correlating with amyloid and tau markers and hippocampal volume. This describes a possible imaging marker of disease progression, not a treatment, cure or prevention.
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Vascular contributions to cognitive impairment and dementia (VCID) are a common cause of cognitive decline, yet limited therapies exist.
Why it matters
This review links cholesterol, atherosclerosis and APOE4 to vascular contributions to cognitive impairment and dementia, noting that few experimental models exist. It is a review of existing literature and does not report a new treatment or prevention result.
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.
- Cerebrospinal fluid tau protein levels and 18F-fluorodeoxyglucose positron emission tomography in the differential diagnosis of Alzheimer's disease
- Oxidized cholesterol as the driving force behind the development of Alzheimer's disease
- [Diagnostic value of tau in cerebrospinal fluid in alzheimer disease]
- Nonsteroidal anti-inflammatory drug use and Alzheimer-type pathology in aging
- Clinical Effect of Early vs Late Amyloid Positron Emission Tomography in Memory Clinic Patients: The AMYPAD-DPMS Randomized Clinical Trial
- Cerebrospinal Fluid β‐Amyloid and τ Levels in Patients With Iatrogenic Cerebral Amyloid Angiopathy, Sporadic Cerebral Amyloid Angiopathy, Alzheimer Disease, and Controls
- Leveraging preclinical models for the development of Alzheimer disease therapeutics
- Brain amyloid imaging
- Improving generalizability and study design of Alzheimer's disease cohort studies in the United States by including under-represented populations
- Longitudinal amyloid imaging using 11C-PiB: methodologic considerations