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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61/100
Patients with moderate to severe AD presented with higher mean (SD) orexin levels compared with controls (154.36 [28.16] vs 131.03 [26.55]; P Conclusions and relevance Our results demonstrate that, in AD, increased cerebrospinal fluid orexin levels are related to a parallel sleep deterioration, which appears to be associated with cognitive decline.
Why it matters
In this case-control study, patients with moderate to severe Alzheimer's disease had higher cerebrospinal fluid orexin levels than controls, and these higher levels were related to worse sleep. It describes a possible link between the orexin system, sleep disruption, and dementia severity, not a treatment or cure.
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Human neurons are functional over an entire lifetime, yet the mechanisms that preserve function and protect against neurodegeneration during ageing are unknown.
Why it matters
REST is induced in normal ageing human neurons but is lost in mild cognitive impairment and Alzheimer's disease, and it represses genes promoting cell death and Alzheimer's pathology while inducing stress response genes. REST protected neurons from oxidative stress and amyloid β-protein toxicity, and conditional deletion of REST in mouse brain led to age-related neurodegeneration, with REST levels during ageing correlated with cognitive preservation and longevity.
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Levels of DDE were 3.8-fold higher in the serum of those with AD (mean [SEM], 2.64 [0.35] ng/mg cholesterol) when compared with control participants (mean [SEM], 0.69 [0.1] ng/mg cholesterol; P Conclusions and relevance Elevated serum DDE levels are associated with an increased risk for AD and carriers of an APOE4 ε4 allele may be more susceptible to the effects of DDE.
Why it matters
This case-control study found that serum levels of the pesticide metabolite DDE were 3.8-fold higher in people with Alzheimer's disease than in controls, and that elevated DDE was associated with increased risk for Alzheimer's disease. It does not show that pesticides cause Alzheimer's disease, and it does not test any treatment or prevention.
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Depressive symptoms in MCI appear to be predictors for progression to AD.
Why it matters
In 183 people with mild cognitive impairment, those with significant depressive symptoms were more likely to progress to Alzheimer's disease. This shows an association between depression and progression but does not show that treating depression changes the risk.
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Key message Extensive variation was observed in conversion rates due to the population sampled, diagnostic criteria, and duration, and because many studies did not account for loss to follow-up.
Why it matters
Across 32 cohort studies, conversion rates from mild cognitive impairment to Alzheimer's dementia varied widely, with annualized rates of about 7.5% to 16.5% in clinic samples and 5.4% to 11.5% in community samples. This shows the range reported in the literature and does not test any treatment.
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Compared with individuals classed as normal, participants with preclinical Alzheimer's disease had an increased risk of death after adjusting for covariates (hazard ratio 6·2, 95% CI 1·1-35·0; p=0·040).
Why it matters
In this 2013 longitudinal cohort study of cognitively normal older people, those classed as having preclinical Alzheimer's disease had a higher risk of death than those classed as normal after adjusting for other factors (hazard ratio 6.2), though the estimate was very uncertain (95% CI 1.1–35.0). The authors also report that preclinical Alzheimer's disease was associated with future cognitive decline, but no figure for this is given in the record. It is an observational association, not proof of cause, and the study did not test any treatment.
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Alzheimer's disease (AD) and Lewy body diseases (LBD), e.g., Parkinson's disease (PD) dementia and dementia with Lewy bodies (DLB), are common causes of geriatric cognitive impairments.
Why it matters
This investigation assessed cerebrospinal fluid α-synuclein and its association with other CSF markers in ADNI participants. It concerns diagnostic and prognostic biomarkers, not treating, curing or preventing Alzheimer's disease.
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The prevalence of dementia in the Western world in people over the age of 60 has been estimated to be greater than 5%, about two-thirds of which are due to Alzheimer's disease.
Why it matters
In whole-genome sequence data from 1,795 Icelanders, the authors report that a rare change in the APP gene, called A673T, "protects against Alzheimer's disease and cognitive decline in the elderly without Alzheimer's disease"; in lab experiments the change cut formation of amyloid-forming peptides by "approximately 40%". The authors present this as "proof of principle for the hypothesis that reducing the β-cleavage of APP may protect against the disease". The summary does not give the size of the protective effect or results from other populations, and this is a finding about an inherited gene variant, not a treatment.
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Core CSF changes in Alzheimer disease (AD) are decreased amyloid β(1-42), increased total tau, and increased phospho-tau, probably indicating amyloid plaque accumulation, axonal degeneration, and tangle pathology, respectively.
Why it matters
This large multicenter study investigated whether age affects how well cerebrospinal fluid biomarkers can diagnose Alzheimer disease, including at the predementia stage. It is a diagnostic performance study and does not test any treatment, cure, or prevention.
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Sixteen men and 24 women diagnosed with Alzheimer's disease participated in the study.
Why it matters
In this randomized trial of 40 people with Alzheimer's disease, those who did a 4-month home exercise program with their carer improved cognition compared with controls. The sample was small, so this suggests exercise may help function but does not show it cures or prevents Alzheimer's disease.
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The National Institute on Aging and the Alzheimer's Association charged a workgroup with the task of developing criteria for the symptomatic predementia phase of Alzheimer's disease (AD), referred to in this article as mild cognitive impairment due to AD.
Why it matters
This paper set out how the National Institute on Aging and the Alzheimer's Association define “mild cognitive impairment due to Alzheimer's disease”, the stage when symptoms have begun but dementia has not. It gives doctors a set of clinical criteria that need no brain scans or spinal-fluid tests, plus a research version for clinical trials that adds those biomarkers and grades a diagnosis at four levels of certainty. It is a definition, not a test of any treatment, and its authors say the biomarker-based criteria still needed validation and standardisation for community use.
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The National Institute on Aging and the Alzheimer's Association charged a workgroup with the task of revising the 1984 criteria for Alzheimer's disease (AD) dementia.
Why it matters
These 2011 expert recommendations revised the 1984 criteria for diagnosing Alzheimer's disease dementia, and were designed to be usable by general healthcare providers without brain scans, spinal-fluid tests or detailed memory testing. The authors state that clinical assessment "will continue to be the cornerstone of the diagnosis in clinical practice"; biomarker evidence was added only "for use in research settings", and they note that "much work lies ahead" to validate it. This is a consensus guideline, not a study that tested patients, and it does not address treatment or prevention.
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A framework for multi-centre MRI studies of Alzheimer's disease has been established consisting of a harmonized MRI acquisition protocol across centres, rigorous QC at both the sites and central data analysis hub and an automated image analysis pipeline.
Why it matters
This paper describes a multi-centre MRI framework for studying Alzheimer's disease, mild cognitive impairment, and healthy controls, with most T1-weighted volumes passing quality control. Measurements of whole brain volume and cortical thickness differed significantly between Alzheimer disease and controls, Alzheimer disease and mild cognitive impairment, and mild cognitive impairment and controls.
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The 59 recruiting sites for the Alzheimer's Disease Neuroimaging Initiative (ADNI).
Why it matters
This cohort study described the characteristics and course of people with mild cognitive impairment and mild Alzheimer's disease who were treated with cholinesterase inhibitors and memantine in the ADNI study. It is observational and does not test whether these drugs cure or prevent Alzheimer's disease.
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Alzheimer's disease is hypothesized to be caused by an imbalance between β-amyloid (Aβ) production and clearance that leads to Aβ accumulation in the central nervous system (CNS).
Why it matters
Using metabolic labeling, the researchers measured how fast amyloid-beta (Aβ42 and Aβ40) is made and cleared in the central nervous system of people with Alzheimer's disease and cognitively normal controls. Clearance was impaired in Alzheimer's disease while production rates did not differ on average, pointing to impaired clearance in the common late-onset form.
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Alzheimer's disease (AD) is classically defined as a dual clinicopathological entity.
Why it matters
An international expert group (the International Working Group for New Research Criteria for the Diagnosis of AD) proposed a shared vocabulary for Alzheimer's, because biomarkers that give "in-vivo evidence of the disease" had led to new research criteria combining a specific pattern of memory and thinking changes with biological evidence of Alzheimer's pathology. Its central proposal is to treat Alzheimer's as "a clinical and symptomatic entity that encompasses both predementia and dementia phases." This is an expert position paper with no patient data, written for researchers and clinicians, and the authors note that the framework has "stimulated debate".
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Lean mass was reduced in persons with early AD compared with controls without dementia (F = 7.73; P = .006) after controlling for sex.
Why it matters
People with early Alzheimer's disease had reduced lean body mass compared with controls without dementia, and lean mass was associated with brain volume and cognitive performance. This describes a body-composition change in early disease and does not show that altering lean mass treats or prevents Alzheimer's disease.
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During a mean follow-up of 3.6 years, 138 persons developed AD.
Why it matters
In this cohort of older people without dementia, greater muscle strength was linked to a lower risk of Alzheimer's disease and slower cognitive decline. This is an association and does not show that strengthening muscles prevents Alzheimer's disease.
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61/100
The single nucleotide polymorphism rs1080985 in the CYP2D6 gene may influence the clinical efficacy of donepezil in patients with mild to moderate Alzheimer disease (AD).
Why it matters
In this study of patients with mild to moderate Alzheimer disease, those carrying a particular CYP2D6 gene variant had a higher risk of responding poorly to donepezil. This concerns predicting response to an existing symptom treatment, not curing or preventing the disease.
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The aim of this observational study was to evaluate whether the treatment of VRF is associated with a slower cognitive decline in patients who have AD without cerebrovascular disease (CVD).
Why it matters
This observational study of 301 Alzheimer's disease patients examined whether treating vascular risk factors was linked to slower cognitive decline. Because it is observational, it can show an association but cannot prove that treating these risk factors causes slower decline.
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MRI and CSF provide complimentary predictive information about time to conversion from amnestic mild cognitive impairment to Alzheimer disease and combination of the 2 provides better prediction than either source alone.
Why it matters
In 399 people from the Alzheimer's Disease Neuroimaging Initiative, both an MRI score of Alzheimer-like brain changes (STAND) and a spinal-fluid ratio of total tau to amyloid-beta 1-42 predicted how soon people with amnestic mild cognitive impairment were diagnosed with Alzheimer's disease (hazard ratios 2.6 and 2.0 per interquartile change). The authors conclude the two give complementary information, with the combination predicting better than either alone, and the MRI score was only "slightly" better at predicting two-year decline. This is a group-level prediction study, not a test for individuals and not evidence about treatment or prevention.
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61/100
Although beta-amyloid (Abeta) plaques are a primary diagnostic criterion for Alzheimer's disease, this pathology is commonly observed in the brains of non-demented older individuals.
Why it matters
In older adults without dementia, higher brain amyloid measured by PET was associated with smaller hippocampus volume and, in some groups, worse episodic memory. This is observational imaging research about how amyloid relates to memory and brain structure, not a treatment or cure.
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The pathologic changes of Alzheimer disease (AD) evolve very gradually over decades before the disease becomes clinically manifest.
Why it matters
In autopsy brains, people with asymptomatic Alzheimer's disease showed significant hypertrophy of neuronal cell bodies, nuclei and nucleoli in the hippocampus and anterior cingulate gyrus compared with control and mild cognitive impairment cases. The authors suggest this hypertrophy may represent an early reaction to the presence of neurotoxic amyloid.
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In this longitudinal study, impaired acute insulin response at midlife was associated with an increased risk of Alzheimer disease (AD) up to 35 years later suggesting a causal link between insulin metabolism and the pathogenesis of AD.
Why it matters
In this long-term study of men, a low insulin response at midlife was associated with a higher cumulative risk of Alzheimer's disease, and impaired glucose tolerance increased the risk of vascular dementia but not Alzheimer's disease. These findings link insulin secretion to risk but do not show that any treatment or prevention targeting insulin changes the course of Alzheimer's disease.
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Patients and their study partners who were enrolled in a clinical trial supported proxy consent both for themselves and as a matter of policy.
Why it matters
This interview study found that patients with Alzheimer's disease and their study partners generally supported proxy consent for clinical trial enrollment. It addresses research enrollment practices and has no implications for treating, curing, or preventing the 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.
- HSV-1 as a Potential Driver of Alzheimer’s Disease
- Diagnostic utility of abbreviated fluency measures in Alzheimer disease and vascular dementia
- Simultaneous resting-state FDG-PET/fMRI in Alzheimer Disease: Relationship between glucose metabolism and intrinsic activity
- Brain properties predict proximity to symptom onset in sporadic Alzheimer's disease
- Is a randomized trial of antioxidants in the primary prevention of Alzheimer disease warranted?
- Factors associated with resistance to dementia despite high Alzheimer disease pathology
- Neuroinflammation and nutrition in Alzheimer’s disease
- Altered expression of diabetes-related genes in Alzheimer's disease brains: the Hisayama study
- Whole-genome sequencing reveals new Alzheimer's disease-associated rare variants in loci related to synaptic function and neuronal development
- Alzheimer disease pathology in cognitively healthy elderly: a genome-wide study