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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Alzheimer's disease (AD) is generally understood as primarily affecting cognition while sparing motor function, at least until the later stages of the disease.
Why it matters
This review reports that people with Alzheimer's disease have a higher prevalence of falls and different walking patterns that increase gait instability, and proposes that executive dysfunction contributes to this fall risk. It suggests a new approach targeting cognition, but no treatment trial is presented.
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49/100
Alzheimer disease (AD) is the most common cause of dementia.
Why it matters
This genomewide screen in an isolated Dutch population genotyped late-onset Alzheimer's disease patients and relatives to look for genetic risk factors. It is a genetic association study and does not show that any intervention treats, cures, or prevents the disease.
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Blood-brain barrier (BBB) impairment is a stable characteristic over 1 year and present in an important subgroup of patients with Alzheimer disease.
Why it matters
In this small biomarker study, blood-brain barrier disruption was present in a subgroup of patients with mild to moderate Alzheimer disease and was stable over one year, correlating with faster progression. It describes a marker of disease course but does not test any treatment.
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Presenilin mutations are the main cause of familial Alzheimer disease.
Why it matters
This paper argues that presenilin mutations, long described as a gain of toxic function, actually cause a partial loss of function in the gamma-secretase complex and can decrease amyloid beta production. It is a reinterpretation of existing data and does not report a new treatment or cure.
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Dominantly inherited mutations in the genes encoding presenilins (PS) and the amyloid precursor protein (APP) are the major causes of familial Alzheimer's disease (AD).
Why it matters
This paper proposes that partial loss of presenilin function, rather than beta-amyloid accumulation alone, may underlie memory loss and neurodegeneration in Alzheimer's disease. It is a hypothesis based on existing evidence and does not report a tested treatment, cure or prevention.
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This review reports correlations between four independent fields related to inflammation and Alzheimer disease: fundamental pathology, epidemiology, transgenic animal studies and clinical trials.
Why it matters
This review reports that long-term users of traditional NSAIDs showed a significant risk reduction or a trend towards it in epidemiological studies, while clinical trials are also discussed. It does not establish NSAIDs as a proven treatment or prevention for Alzheimer's disease.
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Our aim was to investigate the extent of white matter tissue damage in patients with early Alzheimer disease (AD) using diffusion tensor magnetic resonance imaging (DTI).
Why it matters
In 12 patients with early Alzheimer disease, diffusion tensor imaging showed increased diffusivity and decreased fractional anisotropy in several white matter regions compared with controls. This is a small imaging study of white matter damage and does not test any treatment, cure, or prevention.
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These effects were most pronounced in caregivers of subjects with Alzheimer's disease.
Why it matters
In older caregivers of people with Alzheimer's disease, poor sleep was associated with higher plasma levels of the proinflammatory cytokine interleukin-6 and the procoagulant marker fibrin D-dimer. This suggests a mechanism that may explain how disturbed sleep might be linked to cardiovascular risk, particularly in older people under chronic stress.
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Laypersons at heightened risk of Alzheimer disease discriminate among research scenarios of varying risks and burdens.
Why it matters
In a survey of 229 people at heightened risk for dementia, a large majority found minimal risk studies and randomized trials of new medications acceptable for surrogate consent, while a smaller majority found more invasive studies acceptable. This is about attitudes toward research consent, not about treating, curing, or preventing Alzheimer's disease.
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These data provide evidence for clinical and functional heterogeneity among subjects with aMCI and suggest that 18FDG-PET findings combined with memory scores may be useful in predicting short-term conversion to AD.
Why it matters
In this small group of people with amnestic mild cognitive impairment, those who converted to Alzheimer's within a year showed a particular pattern of reduced brain glucose metabolism, and memory scores related to these patterns. This is a small study about identifying who may progress, not about treating, curing, or preventing the disease.
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This potential benefit must be balanced against the possibility that ventricular volumes may be more likely to be affected by factors other than neurodegeneration.
Why it matters
In this small study, patients with Alzheimer disease showed faster ventricular expansion and whole-brain atrophy than controls at both 6 and 12 months. The authors suggest that using the ventricular boundary shift integral could allow disease-modifying effects to be shown with smaller sample sizes in short trials, though ventricular volumes may be affected by factors other than neurodegeneration.
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Brain-derived neurotrophic factor (BDNF) is critical for the function and survival of neurons that degenerate in the late stage of Alzheimer's disease (AD).
Why it matters
In donated brain tissue, a nerve-support protein called BDNF was already lower in people with mild cognitive impairment (mature form down 34%, precursor down 21% versus people without impairment) and lower still in mild-to-moderate Alzheimer's (down 62% and 30%). Lower levels went along with worse scores on memory and thinking tests, which the authors read as a sign that the drop happens early in the disease. This is a one-time comparison of brain tissue: it shows an association, not a cause, and it tested no treatment.
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49/100
Epidemiological studies suggest that individuals with greater education or more cognitively demanding occupations have diminished risk of developing dementia.
Why it matters
In a transgenic mouse model of Alzheimer's disease, enriched housing improved learning and memory, and it normalized the performance of amyloid-beta-overproducing mice to the level of standard-housed nontransgenic mice. These results are in animals and show that amyloid-beta's effects on nervous system function can be strongly modulated by environmental factors, not that enrichment treats or prevents Alzheimer's disease in people.
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We examined how an Alzheimer disease (AD) family history assessment as compared to a risk assessment incorporating the absence of a disease-associated susceptibility allele affected risk perception among adult children with a family history of AD.
Why it matters
This study looked at how people perceived their risk of Alzheimer's disease after receiving different types of risk information. It does not test any treatment and provides no evidence for curing or preventing the disease.
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Just as neuronal activity is essential to normal brain function, microtubule-associated protein tau appears to be critical to normal neuronal activity in the mammalian brain, especially in the evolutionary most advanced species, the homo sapiens.
Why it matters
This review explains that in Alzheimer's disease and other tauopathies, abnormal hyperphosphorylation of tau causes it to lose normal function and gain a toxic function that disrupts microtubules. It describes this as the most established cause of dysfunctional tau, but it does not report a treatment or cure.
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We examined the association of mtDNA variation with Alzheimer disease (AD) risk in Caucasians (989 cases and 328 controls) testing the effect of individual haplogroups and single nucleotide polymorphisms (SNPs).
Why it matters
This genetic study found that mitochondrial haplogroup U was linked to higher Alzheimer disease risk in men and lower risk in women, independent of APOE. It suggests a possible genetic factor but does not offer any treatment, cure, or prevention.
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49/100
Nerve growth factor (NGF) is critical for the regulation, differentiation, and survival of basal forebrain cholinergic neurons that degenerate in the late stage of Alzheimer disease (AD).
Why it matters
In this study, proNGF protein was 1.4-fold greater in the mild cognitive impairment group and 1.6-fold greater in mild to moderate Alzheimer's disease compared with no cognitive impairment, and proNGF levels negatively correlated with Mini Mental Status Examination score. The authors suggest proNGF levels increase during the preclinical stage of Alzheimer's disease and may reflect an early biological marker, but no treatment was tested.
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Amyloid precursor protein (APP), ADAM 10, and beta-site-APP cleaving enzyme (BACE) alterations were evaluated in platelets of 31 patients with Alzheimer disease (AD) and 15 age-matched controls.
Why it matters
This study found significant changes in platelet amyloid precursor protein, ADAM 10 and BACE from the earliest clinically detectable stage of Alzheimer's disease in 31 patients and 15 controls. It suggests these measurements may help with early diagnosis but does not provide a treatment, cure or prevention.
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Alzheimer disease is associated with a significant decrease in CSF beta-amyloid1-42 levels along with an increase in CSF tau levels.
Why it matters
In 131 people with Alzheimer's and 72 controls, cerebrospinal fluid beta-amyloid1-42 was significantly lower and tau significantly higher in Alzheimer's, and set cutpoints gave a sensitivity of 92% and specificity of 89%. A meta-analysis of other studies confirmed an overall difference between the groups. The authors caution that the findings are preliminary and retrospective and the assays are not standardized.
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Recent epidemiological and clinico-pathologic data suggest overlaps between Alzheimer disease (AD) and cerebrovascular lesions that may magnify the effect of mild AD pathology and promote progression of cognitive decline or even may precede neuronal damage and dementia.
Why it matters
This review describes overlaps between Alzheimer's disease and cerebrovascular lesions, including cerebral amyloid angiopathy and microvascular changes that may worsen cognitive decline. It is a review of pathology and does not report a treatment, cure, or prevention.
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Subcortical lacunes were not related to cognitive measures independent of effects of other MRI variables.
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Alzheimer's disease (AD) is a devastating dementia of late life that is correlated with a region-specific neuronal cell loss.
Why it matters
This study examines the theory that neurons degenerate in Alzheimer's disease because they reenter a lethal cell cycle. It provides direct proof for DNA replication preceding neuronal cell death, supporting this theory.
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The authors performed a 6-week, randomized, double-blind, placebo-controlled, parallel-group trial of carbamazepine (400 mg/day) with 21 agitated subjects (16 completers) who had been treated unsuccessfully with antipsychotics.
Why it matters
In this 6-week pilot randomized trial of 21 agitated outpatients with Alzheimer disease who had not responded to antipsychotics, carbamazepine showed modest clinical benefit, with particular benefit for hostility. The authors describe the effect on global ratings as similar to an earlier report in nursing home residents, and the trial was small.
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There is a lower prevalence of diagnosed probable AD in patients taking 2 different 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors-lovastatin and pravastatin.
Why it matters
In hospital records, the prevalence of diagnosed probable Alzheimer disease was 60% to 73% lower among patients taking statins (lovastatin and pravastatin) than in the total patient population or in patients taking other blood pressure or heart medicines. The authors say causes cannot be inferred from these data and the association warrants further study.
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Severe CAA confers a greater risk of VLs in AD, even within strata of APOE genotype.
Why it matters
In 306 autopsy-confirmed Alzheimer's cases from the UC San Diego brain series, vascular lesions were found in 33% of brains with severe cerebral amyloid angiopathy versus 19% with mild or no CAA, and the gap persisted within APOE genotype groups (47% vs 9.5% among APOE4/4 carriers). The authors conclude the CAA–lesion link "is not a spurious one owing to APOE4," and they point to it as relevant to "mixed" Alzheimer's/vascular dementia. This is an after-death association study; it does not show cause or test any treatment.
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.
- Global, Regional, and National Disparities in the Burden of Alzheimer’s Disease and Other Dementias, 1990–2021
- Subjective memory decline predicts greater rates of clinical progression in preclinical Alzheimer's disease
- Predicting Mild Cognitive Impairment to Alzheimer's Disease Progression by Explainable Multi‐Modal Framework Using Deep and Machine Learning Hybrid Model
- Management of agitation and aggression associated with Alzheimer disease
- Investigating Potential Alzheimer's Disease Therapies through an Agent-Based Model of Impaired Microglia MetabolismModeling Impaired Microglia Metabolism
- Rivastigmine for Alzheimer's disease
- The role of mitochondria in Alzheimer's disease
- The Alzheimer amyloid precursor protein maps to human chromosome 21 bands q21.105-q21.05
- Neuropsychiatric signs and symptoms of Alzheimer's disease: New treatment paradigms
- Cerebral microhemorrhage and brain β-amyloid in aging and Alzheimer disease