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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Our data indicate that the retinal nerve fiber layer degeneration is paralleled with dementia progression.
Why it matters
Retinal nerve fiber layer thickness decreased gradually from mild cognitive impairment to severe Alzheimer's disease compared with controls. The authors suggest monitoring this thickness may help assess disease progression and treatment effects, but this study did not test any treatment.
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Treatments were generally well tolerated and adverse events (AEs) were seen at similar rates across all treatment groups, with the exception that more injection site reactions were seen in the groups with a higher level of adjuvant.
Why it matters
In this phase 2 trial of 332 patients with early Alzheimer's disease, the control preparation unexpectedly showed significant effects on several clinical outcomes rather than the AD02 vaccine. This does not provide evidence that AD02 treats Alzheimer's disease.
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Pathogenic mutations in the amyloid precursor protein (APP) gene have been described as causing early onset familial Alzheimer disease (AD).
Why it matters
This laboratory study examined how the rare A673T variant of amyloid precursor protein confers protection against Alzheimer's disease. It is basic molecular research into a protective gene variant and does not provide a treatment or cure.
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Alzheimer's disease (AD) is a neurodegenerative disease leading to a progressive and irreversible loss of mental functions.
Why it matters
In a small group of 25 Algerian patients, levels of the inflammatory cytokines IFN-γ and TNF-α and production of nitric oxide differed across stages of Alzheimer's disease and mild cognitive impairment. This is an early study of immune and oxidative processes and does not test any treatment.
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44/100
Clinical trials to advance the diagnosis and treatment of Alzheimer disease (AD) may expose research subjects to discrimination risks.
Why it matters
This paper discusses how people enrolled in Alzheimer's research using amyloid PET or spinal fluid amyloid measures could face discrimination from insurers and employers, and that current laws do not protect against this. It calls for policy and record-keeping changes to protect research participants, but it does not test any treatment or prevention.
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Many trials of drugs aimed at preventing or clearing β-amyloid pathology have failed to demonstrate efficacy in recent years and further trials continue with drugs aimed at the same targets and mechanisms.
Why it matters
This paper discusses tau aggregation as a target for Alzheimer's therapy, noting that truncated tau can convert normal tau into aggregated forms that spread to neighbouring neurons and that tau aggregation can begin in midlife. It presents a rationale for tau-aggregation inhibitor therapy but does not report a proven treatment.
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Alzheimer's disease (AD) is the most common type of dementia accounting for 60-80% of the reported cases.
Why it matters
Comparing blood from 21 treated Alzheimer's patients with 10 controls, researchers found higher inflammation and oxidative stress markers, including IL-6, TNF-α and homocysteine, and lower antioxidant defences in the patients. Profiles differed by medication, with IL6 47% lower in the Rivastigmine-treated group than in other patients. The authors note the small group size and see the results as a basis for future studies on how medicines and diet affect these markers.
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Neurofibrillary tangles, one of the hallmarks of Alzheimer disease (AD), are composed of paired helical filaments of abnormally hyperphosphorylated tau.
Why it matters
This laboratory study used an unbiased approach to screen 352 human kinases for their ability to phosphorylate tau at sites associated with Alzheimer disease, in order to identify possible targets. It is early cell-based work and does not test any treatment, cure, or prevention in people.
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This study presents the Edinburgh Cognitive and Behavioural ALS Screen (ECAS), developed for ALS patients with physical disability for use by health care professionals.
Why it matters
This study presents a screening tool (the ECAS) for detecting cognitive and behavioral changes in people with ALS, and found language and executive deficits in some patients. It is about assessment in ALS, not about treating, curing or preventing Alzheimer's disease.
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The University of Minnesota Medical School in Minneapolis, Minnesota, and the Salhgrenska University Hospital, Sweden.
Why it matters
This study measured two specific amyloid-beta oligomers in cerebrospinal fluid and examined their relationship to tau in cognitively normal older adults, people with mild cognitive impairment, and people with Alzheimer's disease. It is early observational work and does not test any treatment, cure, or prevention.
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44/100
Recent works have demonstrated a rare functional variant (R47H) in triggering receptor expressed on myeloid cells (TREM) 2 gene, encoding TREM2 protein, increase susceptibility to late-onset Alzheimer's disease (AD), with an odds ratio similar to that of the apolipoprotein E ε4 allele.
Why it matters
This review describes how the rare TREM2 R47H variant increases susceptibility to late-onset Alzheimer's disease and how TREM2 may suppress inflammatory responses. It is a review of existing evidence and does not show any treatment, cure or prevention.
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In the 3 studies combined, the data indicated that rofecoxib more than tripled the risk of confirmed CVT death (risk ratio = 3.57 [1.48-9.72], P = .004).
Why it matters
This analysis of three rofecoxib trials in Alzheimer's disease found the drug more than tripled the risk of confirmed cardiovascular thrombotic death compared with placebo. This shows harm from rofecoxib rather than any benefit for treating or preventing Alzheimer's disease.
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Alzheimer's disease (AD) is a highly complex neurodegenerative disorder of the aged that has multiple factors which contribute to its etiology in terms of initiation and progression.
Why it matters
This review summarizes several proposed explanations for Alzheimer's disease, including amyloid-beta accumulation, the cholinergic hypothesis, neuroinflammation and the calcium hypothesis, and discusses melatonin. It does not establish a treatment or cure.
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There is increasing evidence that deficient clearance of β-amyloid (Aβ) contributes to its accumulation in late-onset Alzheimer disease (AD).
Why it matters
This paper reviews amyloid-beta-degrading enzymes that reduce amyloid-beta levels and protect against cognitive impairment in mouse models of Alzheimer's disease. The evidence comes from animal models, and the age- and disease-related changes in expression of some of these enzymes remain to be determined.
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The prevalence of postoperative cognitive disturbance, coupled with growing in vitro, cell, and animal evidence suggesting anesthetic effects on neurodegeneration, calls for additional study of the interaction between surgical care and Alzheimer neuropathology.
Why it matters
This study measured cerebrospinal fluid biomarkers in only 11 patients undergoing surgery for nasal CSF leak, to look at whether anesthesia and surgery affect Alzheimer-related markers. The sample is very small and preliminary, and no treatment, cure, or prevention is shown.
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44/100
The results of this study suggest that dyslipidemia increases the risk of plaque-type pathology.
Why it matters
Among 147 residents of Hisayama, Japan, whose cholesterol was measured in 1988 and whose brains were examined at autopsy in 1998–2003, people with brain plaques had had higher total and LDL cholesterol and related ratios, even when plaques were sparse to moderate and after accounting for APOE ε4. The study found "no relationship between any lipid profile" and tangles, the other hallmark of Alzheimer's. It is an association in one community and does not show that lowering cholesterol prevents plaques or dementia.
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Superoxide production via NADPH-oxidase (NOX) has been shown to play a role in a variety of neurological disorders, including Alzheimer disease (AD).
Why it matters
This study found that NADPH-oxidase enzyme activity was elevated in the brain tissue of people with mild cognitive impairment and Alzheimer's disease compared to those with no cognitive impairment. The findings describe a biological change associated with disease progression but do not test any treatment or prevention.
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We applied an automated hippocampal segmentation technique based on adaptive boosting (AdaBoost) to the 1.5 T magnetic resonance imaging (MRI) baseline and 1-year follow-up data of 243 subjects with mild cognitive impairment (MCI), 96 with Alzheimer's disease (AD), and 145 normal controls (NC) scanned as part of the Alzheimer's Disease Neuroimaging Initiative (ADNI).
Why it matters
This study found that a mother's history of dementia was linked to greater hippocampal shrinkage in people with mild cognitive impairment and Alzheimer's disease, independent of the ApoE4 gene. It does not show that any treatment or prevention can change this risk.
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Low cerebrospinal fluid (CSF) amyloid-beta(1-42) concentration and high total-tau/Abeta(1-42) ratio have been recommended to support the diagnosis of prodromal Alzheimer's disease (AD) in patients with amnestic mild cognitive impairment (aMCI) and also to select patients for clinical trials (Shaw et al, Ann Neurol 2009;65:403-13; Dubois et al, Lancet Neurol 2007;6:734-46).
Why it matters
Using clinical trial simulations, this study found that requiring a low cerebrospinal fluid amyloid-beta 1-42 level to enroll patients with amnestic mild cognitive impairment did not make trials more efficient. This is a methodological finding about trial design, not evidence about treating or preventing Alzheimer disease.
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Alzheimer disease (AD) is one of the most prevalent chronic medical conditions affecting the elderly population.
Why it matters
Data suggest that specifically designed cognitive interventions could provide therapeutic benefits to patients with Alzheimer's disease associated with biological changes in the brain. Evidence also indicates that combining pharmacological and non-pharmacological interventions could provide greater relief of clinical symptoms than either alone.
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44/100
A growing body of epidemiological evidence suggested that metabolic syndrome (MetS) and Mets components (impaired glucose tolerance, abdominal or central obesity, hypertension, hypertriglyceridemia, and reduced high-density lipoprotein cholesterol) may be important in the development of age-related cognitive decline (ARCD), mild cognitive impairment (MCI), vascular dementia, and Alzheimer's disease (AD).
Why it matters
This review suggests that metabolic syndrome and its components may be important in the development of cognitive decline and Alzheimer's disease, and discusses how they may influence amyloid and tau pathology. It says future trials could test whether modifying these components lowers the risk of cognitive decline, so no treatment or prevention is established here.
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Alzheimer's disease (AD) is an age-related neurodegenerative disorder.
Why it matters
This review reports that markers of lipid peroxidation such as HNE are increased in the brains of people with Alzheimer's disease and mild cognitive impairment. It suggests that lipid-accessible antioxidant molecules could be a promising therapeutic approach to treat or slow progression of mild cognitive impairment and Alzheimer's disease, but no treatment was tested here.
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The groups of individuals who agreed to participate in the imaging substudies of AD trials were remarkably comparable to the comparison groups at baseline on a wide range of demographic and clinical measures; there seems to be a minimal effect of self-selection bias.
Why it matters
This study compared participants who enrolled in MRI substudies of Alzheimer's trials with those who did not, and found they were largely similar at baseline. It addresses whether imaging substudy samples are representative, not whether any treatment works.
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In a population-based sample, increasing gliosis precedes development of Alzheimer lesions.
Why it matters
In a population-based sample, GFAP increased with increasing Braak stage, even at early stages, but within Braak stages GFAP did not differ between demented and non-demented individuals, and it was not independently predictive of dementia. This suggests that astrogliosis is not solely driven by Alzheimer lesions and does not by itself predict dementia.
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Peripheral benzodiazepine receptor (PBR) in the brain of Alzheimer's disease (AD) patients has been discussed in relation to the role of gliosis in AD.
Why it matters
This PET study with [11C]DAA1106 found increased binding of peripheral benzodiazepine receptor in 10 Alzheimer's disease patients compared with 10 age-matched controls. It reports no treatment, cure, 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.
- Alzheimer's disease: risk factors and potentially protective measures
- The future of Alzheimer's disease: the next 10 years
- Clinical efficacy and safety of donepezil on cognitive and global function in patients with Alzheimer's disease. A 24-week, multicenter, double-blind, placebo-controlled study in Japan. E2020 Study Group
- Cardiovascular Risk as a Moderator of the Relationship Between Plasma Alzheimer Disease Biomarkers and Cognitive Status
- A mass-producible macaque model displays a durable Alzheimer-like cognitive deficit and hallmark amyloid-β/tau/neurofilament light chain pathologies
- U1 small nuclear ribonucleoprotein complex and RNA splicing alterations in Alzheimer's disease
- Biomarkers of Alzheimer disease in plasma
- Amyloid Hypothesis: Is There a Role for Antiamyloid Treatment in Late-Life Depression?
- Treatment with a C5aR antagonist decreases pathology and enhances behavioral performance in murine models of Alzheimer's disease
- Neuropsychiatric symptoms and progression to pathologically confirmed Alzheimer’s disease