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) drug developments and clinical trials (CT) remain vulnerable to problems that undermine research validity.
Why it matters
This review argues that many Alzheimer's disease drug trials fail because of problems such as inaccuracy, imprecision, bias, inter-site variance and lack of homogeneous sampling, which reduce the ability to detect drug-placebo differences. The authors propose that researchers should privilege biomarkers and develop them as surrogate targets for preventive treatment, but no specific treatment is tested or shown to work.
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Mild cognitive impairment (MCI) is regarded as the prodromal stage of dementia disorders, such as Alzheimer's disease (AD).
Why it matters
Among people with mild cognitive impairment, those with abnormal CSF tau and amyloid performed worse on speed, attention and memory tests than those with normal biomarker levels. This supports using CSF biomarkers plus cognitive testing to identify who is more likely to be on an Alzheimer's path, but it does not test any treatment.
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Numerous studies have shown a marked decrease of beta-amyloid(42) (Abeta(42)) in the cerebrospinal fluid (CSF) of patients with incipient Alzheimer's disease (AD).
Why it matters
Plasma amyloid-β isoforms did not differ between people with mild cognitive impairment who later developed Alzheimer's disease and those who did not, and plasma levels did not predict progression. Low cerebrospinal fluid Abeta(1-42) was strongly associated with increased risk of future Alzheimer's disease, so cerebrospinal fluid biomarkers were better predictors than plasma amyloid-β in this study.
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A well-documented feature of Huntington's disease (HD) is disproportionate impairment in the ability to recognise the emotional expression of disgust.
Why it matters
In small groups of patients, both Huntington's disease and frontotemporal dementia showed impaired emotion recognition compared with controls, with different patterns across emotions. This is a small comparative study of emotion processing and does not test any treatment, cure, or prevention for Alzheimer's disease.
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The major molecular risk factor for Alzheimer disease so far identified is the amyloidogenic peptide Abeta(42).
Why it matters
Lowering cholesterol inhibited both beta-secretase and gamma-secretase, the two enzymatic activities responsible for amyloid-beta production, additively in the cellular context studied. This is laboratory work on a mechanism and does not show that lowering cholesterol treats or prevents Alzheimer disease.
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The increasing prevalence of Alzheimer's disease and the devastating consequences of late-life dementia motivates the drive to develop diagnostic biomarkers to reliably identify the pathology associated with this disorder.
Why it matters
This paper reviews strategies for developing biomarkers to detect Alzheimer's pathology early, including cerebrospinal fluid tau and amyloid, structural MRI, MRI T(1)rho, and amyloid PET or SPECT imaging. It discusses diagnosis and possible measures of treatment efficacy, but it does not itself test a treatment, cure, or prevention.
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Adults with Down syndrome (DS) develop Alzheimer disease (AD) pathology progressively with age but clinical signs of dementia are delayed by at least 10 years after the first signs of disease.
Why it matters
Adults with Down syndrome develop Alzheimer's brain changes with age, but dementia is delayed by at least 10 years and some never develop it despite extensive pathology. This paper proposes that genes overexpressed in Down syndrome (APP, DSCAM, MNB/DYRK1A and RCAN1) may help the ageing brain compensate, and that supporting such compensation, which animal intervention studies suggest may be beneficial, could be explored in Down syndrome as a route to healthier brain ageing in the general population.
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Standard markers in cerebrospinal fluid (CSF), as soluble amyloid beta 1-42 (Abeta1-42) and total tau protein (t-tau), may contribute to dementia subtypes diagnostic accuracy.
Why it matters
This study analyzed Aβ1-42 and total tau cerebrospinal fluid levels across groups of Alzheimer's disease patients with different degrees of cognitive impairment. It found these markers were not related to the different degree of cognitive impairment, and it concerns diagnosis rather than treatment, cure, or prevention.
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Neprilysin (NEP) degrades amyloid-beta (Abeta) and is thought to contribute to its clearance from the brain.
Why it matters
This study found that neprilysin enzymatic activity was significantly reduced in Alzheimer's disease and that low neprilysin levels were a significant independent predictor of moderate to severe cerebral amyloid angiopathy. It describes a possible mechanism related to amyloid clearance and does not test any treatment, cure, or prevention.
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Alzheimer disease is a progressive dementia with unknown etiology that affects a growing number of the aging population.
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The prevention of Alzheimer disease (AD) remains an important goal because of its high prevalence in our society and its associated costs.
Why it matters
This paper reviews primary prevention trials for Alzheimer disease and notes that no primary prevention trial has successfully delayed the development of the disease to date. It discusses the difficulties of conducting such trials, not a proven prevention method.
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41/100
Dementia and age-related macular degeneration (AMD) are major causes of disability in the elderly. n-3 Fatty acids, particularly docosahexaenoic acid (DHA), are highly concentrated in brain and retinal tissue and may prevent or delay the progression of dementia and AMD.
Why it matters
This paper discusses whether dietary n-3 fatty acids, especially DHA from fish and fish oils, might prevent or delay dementia and age-related macular degeneration. It states that firm recommendations cannot yet be made, so it does not establish any prevention benefit.
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Alzheimer's dementia (AD) is a chronically progressive neurodegenerative disease.
Why it matters
This paper describes how copper metabolism may relate to Alzheimer's disease, noting that copper levels are changed in patients and mouse models. In mice, oral copper supplements restored brain copper, reduced amyloid-beta production, and reduced mortality, and a human trial in mild Alzheimer's was underway at the time.
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Oxidative stress is extensive in Alzheimer disease (AD) brain.
Why it matters
This review discusses evidence that amyloid beta-peptide(1-42) causes oxidative stress and neurotoxicity and that mutations increasing its production lead to early-onset Alzheimer's disease. It proposes a central role for this peptide in disease but reports no treatment or cure.
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White matter hyperintensities (WMH) on MRI scans indicate lesions of the subcortical fiber system.
Why it matters
This study measured the regional distribution of white matter hyperintensities on MRI in 20 vascular dementia patients, 25 Alzheimer's disease patients and 22 healthy elderly subjects. It describes imaging differences between groups and does not test any treatment, cure or prevention.
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A change of the prion protein conformation results in a class of neurodegenerative diseases called the transmissible spongiform encephalopathies (like mad cow and Creutzfeld-Jakob diseases).
Why it matters
This review discusses the bioinorganic chemistry of copper and metal binding by the prion protein and amyloid precursor protein in neurodegeneration. It is a chemistry review and does not test any treatment, cure, or prevention.
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The extracellular accumulation of amyloid-beta (Abeta) in neuritic plaques is one of the characteristic hallmarks of Alzheimer's disease (AD), a progressive dementing neurodegenerative disorder of the elderly.
Why it matters
This review describes how beta-amyloid binds to lipids, proteins and proteoglycans on neuronal and glial membranes, which can promote amyloid fibrillation, damage membranes and trigger local inflammation. It is a summary of laboratory findings about binding and toxicity, not a study of a treatment or cure in patients.
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Alzheimer disease is not a single disorder.
Why it matters
This review proposes that disturbed insulin signal transduction may be a central and early event in sporadic Alzheimer's disease, alongside other risk factors such as aging. It offers therapeutic implications only as discussion and does not establish any treatment, cure, or prevention.
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41/100
Allostasis designates processes of bodily adaptation to stressful challenges, whereas allostatic load means the costs of wear and tear to the body as a consequence of inefficient allostasis.
Why it matters
In 37 spousal Alzheimer caregivers, the number of negative life-events correlated with a procoagulant stress response measured as allostatic load. This concerns caregiver stress biology and cardiovascular risk, not the treatment, cure or prevention of Alzheimer's disease.
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Studies of amyloid precursor protein transgenic mice suggest that immune responses to amyloid beta peptide (Abeta) may be instrumental in the removal of plaques from the brain, but the initial clinical trial of an Abeta vaccine in patients with Alzheimer s disease (AD) was halted as the result of serious neurological complications in some patients.
Why it matters
This study found that Alzheimer's disease patients had elevated serum antibodies to amyloid-beta and that these antibodies enhanced the peptide's neurotoxicity in laboratory tests. It raises concerns about amyloid-beta vaccine approaches and does not establish a treatment, cure, or prevention.
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A multitiered strategy was adopted to assess tau conformational changes within fibrillar lesions during the progression of Alzheimer's disease (AD).
Why it matters
In brain tissue from 37 clinically staged cases, the presence of granulovacuolar and fibrillar lesions correlated with several measures of episodic memory, and tau conformational changes were documented in sequence during Alzheimer's disease. The authors say these conformational changes correlated with episodic memory deficits.
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Active immunization with the human amyloid peptide (Abeta42) or passive immunization with anti-Abeta42 antibodies protects mice that express a mutant human amyloid precursor protein (APP) transgene from cerebral amyloid deposits.
Why it matters
Because anti-amyloid antibodies protect mouse models from amyloid deposits, this study measured natural anti-Aβ42 antibodies in the blood of people with late-onset Alzheimer's and of healthy elderly controls. Controls had significantly higher levels, and IgG antibodies distinguished patients from controls among people without the APOE4 allele. This fits the authors' idea that a high level of these antibodies may protect against Alzheimer's, though it shows a link, not proof.
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In 6-month trials, measurement error makes a substantial contribution to the variance in ADAS-Cog change scores.
Why it matters
This analysis of 536 patients with Alzheimer's disease in placebo groups of drug trials found that those with moderate dementia declined 84% more on the ADAS-Cog total score over 26 weeks than those with milder dementia. The study also found that measurement error substantially contributes to score changes, which is important for designing future trials but does not test any treatment.
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Apolipoprotein E (apoE) and apoE-derived proteolytic fragments are present in amyloid deposits in Alzheimer disease (AD) and cerebral amyloid angiopathy (CAA).
Why it matters
In brain tissue from five people with Alzheimer disease, different fragments of apolipoprotein E were found in amyloid plaques and blood vessels, with plaque cores containing the entire protein and outer regions containing only a C-terminal fragment. This suggests apoE may be involved in how amyloid beta aggregates, but it is a small tissue study and does not offer a treatment.
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Both DLB and DAT groups exhibited impaired performance across the range of tasks designed to assess semantic memory.
Why it matters
In small groups of patients with dementia with Lewy bodies and dementia of Alzheimer's type matched for age and MMSE, both groups showed impaired performance on tasks of semantic memory. This describes similarities in cognitive impairment between the two dementias, but it does not test any treatment 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.
- A meta-analysis investigating the relationship between inflammation in autoimmune disease, elevated CRP, and the risk of dementia
- Multisite study of the relationships between antemortem [ 11 C]PIB‐PET Centiloid values and postmortem measures of Alzheimer's disease neuropathology
- Multi-dimensional attention framework for personalized Alzheimer’s disease progression prediction across sporadic and genetic risk cohorts
- Apolipoprotein E status as a predictor of the development of Alzheimer's disease in memory-impaired individuals
- The Occurrence of Obstructive Sleep Apnea and Its Association With Alzheimer Dementia in Medicaid-Enrolled Adults With Down Syndrome, 2011-2019
- Interpreting the clinical significance of capacity scores for informed consent in Alzheimer disease clinical trials
- Study protocol for the Alzheimer and music therapy study: An RCT to compare the efficacy of music therapy and physical activity on brain plasticity, depressive symptoms, and cognitive decline, in a population with and at risk for Alzheimer's disease
- Association of brain amyloid-β with cerebral perfusion and structure in Alzheimer's disease and mild cognitive impairment
- Association between severe cerebral amyloid angiopathy and cerebrovascular lesions in Alzheimer disease is not a spurious one attributable to apolipoprotein E4
- A phase 2 double-blind placebo-controlled 24-week treatment clinical study of the p38 alpha kinase inhibitor neflamapimod in mild Alzheimer's disease