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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A number of in vivo neurochemistry and neuroimaging techniques, which can reliably assess aspects of physiology, pathology, chemistry, and neuroanatomy, hold promise as biomarkers.
Why it matters
This 2008 review looked at which chemical and brain-imaging measurements, taken in living people, could serve as biomarkers of Alzheimer's disease, and reports that a number of these techniques 'hold promise as biomarkers.' On blood tests it found that studies of plasma amyloid-beta 'are not entirely consistent,' though 'recent findings suggest that decreased plasma Abeta42 relative to Abeta40 might increase the risk of AD' — a possible risk signal, not a diagnosis. It summarises earlier research rather than reporting new data, and the abstract we hold does not name which specific markers the authors judged most promising.
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Oxidative stress is thought to play a role in the pathogenesis of Alzheimer's disease (AD) and increased oxidative DNA damage has been observed in brain tissue from AD patients.
Why it matters
Brain tissue from 10 people with Alzheimer's disease and 9 with amnestic mild cognitive impairment showed reduced DNA base excision repair activity, linked to limited damage processing by DNA glycosylases and reduced DNA synthesis by polymerase beta. The authors suggest this repair defect is a general feature of Alzheimer's brains that may occur early in the disease.
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Metabolic syndrome is associated with Alzheimer disease in elderly subjects.
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Patients with Alzheimer disease have reduced levels of sRAGE in plasma compared with patients with vascular dementia and controls.
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The concept of mild cognitive impairment (MCI) draws attention to cognitive changes not severe enough to warrant the diagnosis of dementia.
Why it matters
This paper proposes that Alzheimer's disease can already be identified before full dementia appears, using specific neuropsychological tests, neuroimaging, and biomarkers. It puts forward diagnostic criteria for 'prodromal AD' but does not report testing a treatment or cure.
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52/100
Cerebrospinal fluid (CSF) concentrations of amyloid beta peptides ending at positions 42 and 40 (Abeta42 and Abeta40, respectively), and total tau (tTau) protein were measured by ELISA in order to compare their accuracy in discriminating patients with Alzheimer's disease (AD, n = 22), non-Alzheimer dementia (nAD, n = 11) and control subjects (CON, n=35).
Why it matters
In a small sample of 22 Alzheimer patients, 11 with other dementias, and 35 controls, this study compared cerebrospinal fluid amyloid-beta 42, amyloid-beta 40, and total tau for telling the groups apart. The amyloid-beta 42/40 ratio classified more patients correctly than amyloid-beta 42 alone, but this is a diagnostic finding only and says nothing about treatment, cure, or prevention.
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Neuroimaging is valuable in predicting future development of AD in patients with MCI and in carriers of the ApoE epsilon 4 allele who are at a higher risk of developing AD than are cognitively normal elderly individuals.
Why it matters
Brain imaging can help predict future Alzheimer's disease in people with mild cognitive impairment and in APOE ε4 carriers, with hippocampal volume on MRI linked to later development of the disease. Longitudinal decreases in brain and hippocampal volume, NAA levels, glucose metabolism, and blood flow were associated with the rate of cognitive decline in Alzheimer's patients.
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52/100
Low n-3 polyunsaturated fatty acid (PUFA) status may be associated with neuro-degenerative disorders, in particular Alzheimer's disease, which has been associated with poor dietary fish or n-3 PUFA intake, and low docosahexaenoic acid (DHA) status.
Why it matters
This case-control study compared serum cholesteryl ester-docosahexaenoic acid levels in patients with Alzheimer's disease. It is an observational biomarker study and does not test whether changing n-3 PUFA intake treats, cures or prevents Alzheimer's disease.
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The purpose of this study was to assess the cross-sectional prevalence and characteristics of anxiety among patients with Alzheimer's disease (AD), as compared with patients with frontotemporal dementia (FTD), patients with vascular dementia (VaD), and normal control subjects.
Why it matters
This cross-sectional study compared anxiety in patients with Alzheimer's disease, frontotemporal dementia, vascular dementia, and normal controls using the Neuropsychiatric Inventory anxiety subscale. It describes how common and what anxiety looks like in these patients but does not test any treatment, cure, or prevention.
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Recently, we demonstrated a significant increase of an oxidized nucleoside derived from RNA, 8-hydroxyguanosine (8OHG), and an oxidized amino acid, nitrotyrosine in vulnerable neurons of patients with Alzheimer disease (AD).
Why it matters
In brain neurons from people with Alzheimer's disease, two markers of oxidative damage were highest early in the disease and lower with longer illness and more plaques and tangles; neurons with tangles had 40%–56% lower relative levels of oxidised RNA (8OHG) than tangle-free neurons. Unexpectedly, more amyloid deposition was associated with less oxidative damage, especially in ApoE ε4 carriers, which the authors suggest may reflect compensatory changes. These are associations from a single measurement per person, so they do not show that oxidative damage causes Alzheimer's or that antioxidants would prevent or treat it.
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52/100
The double dissociation in performance on semantic memory and attention/executive function clearly separated the temporal and frontal variants of FTD and aids the early differentiation of FTD from AD.
Why it matters
This small comparison of patients with early Alzheimer-type dementia and two variants of frontotemporal dementia found distinct patterns of thinking problems that helped tell the conditions apart. It is about diagnosis, not about treating, curing, or preventing Alzheimer's disease.
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1. Of the neurodegenerative diseases that cause dementia, Alzheimer's disease (AD) is the most common.
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Why it matters
Reports a membrane-anchored aspartyl protease with Alzheimer's disease β-secretase activity.
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In common with Alzheimer's disease and vascular dementia, PVHs and WMHs were significantly more extensive in dementia with Lewy bodies than in controls.
Why it matters
White matter changes on MRI were more severe in all dementia groups than in controls and were worse in vascular dementia than in dementia with Lewy bodies or Alzheimer's disease. This is about imaging features that accompany different dementias, not about treating, curing, or preventing Alzheimer's disease.
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In participants with no epsilon4 alleles, the age-specific prevalence of AD reached a maximum and then declined after age 95.
Why it matters
In 5,677 older residents of Cache County, Utah, the share of people with Alzheimer's disease rose with age, peaked and then declined, and the peak came earlier with more copies of APOE-ε4: about age 95 with none, 87 with one, and 73 with two. Being female was linked to Alzheimer's only among ε4 carriers, and the study attributes 70% of the population's attributable risk to ε4. This is a one-time prevalence survey of a single long-lived community that describes associations; it does not show individual risk or onset ages, and it tests no treatment or prevention.
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Selegiline has a long-term beneficial effect in Alzheimer's disease on memory modalities that reflect the function of the prefrontal areas of the brain, which are rich in dopamine receptors.
Why it matters
This 24-week trial of selegiline in 173 nursing-home residents with mild to moderate Alzheimer's disease did not find clear benefit on the measured outcomes. It provides no support for selegiline as a treatment to slow or prevent Alzheimer's disease.
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A central tenet of Alzheimer disease (AD) is the loss of cortical cholinergic function and cholinergic markers in postmortem brain specimens.
Why it matters
This post-mortem study asked whether cholinergic deficits in Alzheimer's disease come before, after, or at the same time as the earliest signs of cognitive decline. It does not report a treatment, cure, or prevention, and its findings are based on brain tissue examined after death.
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Mutations in the amyloid precursor protein (APP) gene cause early-onset familial Alzheimer disease (AD) by affecting the formation of the amyloid beta (A beta) peptide, the major constituent of AD plaques.
Why it matters
Two transgenic mouse lines expressing mutant human amyloid precursor protein developed Alzheimer's-like pathology, including amyloid-beta deposition in the brain. This was an animal study, so it does not directly provide a treatment or cure for human Alzheimer's disease.
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Why it matters
An editorial on consensus recommendations for diagnosing Alzheimer disease after death, from a working group on criteria for neuropathological assessment. It concerns how the diagnosis is confirmed in brain tissue, which supports consistent research but treats nobody.
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This study investigated the frequency and progression of Alzheimer-related lesions, specifically amyloid deposits and intraneuronal neurofibrillary changes, across different age categories.
Why it matters
Reports how often the stages of Alzheimer-related brain lesions appear across different age groups. It describes how pathology is distributed by age, not a treatment or a way to prevent the disease.
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This study examined evidence regarding the oxidative stress hypothesis in Alzheimer's disease.
Why it matters
Discusses the oxidative stress hypothesis in Alzheimer's disease.
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Alzheimer's disease (AD) lesions are characterized by the presence of numerous inflammatory proteins.
Why it matters
Pooling case-control studies, the authors found arthritis and anti-inflammatory drug use were associated with a lower chance of Alzheimer's, for example an odds ratio of 0.556 for arthritis. They suggest anti-inflammatory drugs may protect against Alzheimer's but say controlled clinical trials are needed to test this.
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Several studies have reported an association of the apolipoprotein E allele epsilon 4 (APOE*4) to familial and sporadic late-onset Alzheimer's disease (LOAD).
Why it matters
This population-based study found that the APOE*4 allele was more common in people with early-onset Alzheimer's disease than in controls, and that risk was especially increased in those who inherited two copies. It identifies a genetic risk factor only and does not provide a treatment, cure, or prevention for Alzheimer's disease.
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We surveyed 1,545 subjects--recruited into the UK Medical Research Council elderly hypertension treatment trial between 1982 and 1987--to detect incident cases of dementia, identifying 50 cases of dementia, including 31 cases of probable or possible Alzheimer's disease (AD).
Why it matters
This case-control study confirmed that a family history of dementia and advanced age were associated with dementia and Alzheimer's disease, and found near-significant associations with several cardiovascular risk factors among subjects without a family history. It identifies possible risk factors but does not test any treatment, cure, or prevention.
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Cerebral amyloid angiopathy is a common cause of spontaneous lobar hemorrhage in elderly patients.
Why it matters
This report describes seven patients with cerebral amyloid angiopathy who presented without major lobar hemorrhage, either with recurrent transient neurologic symptoms or rapidly progressive dementia. It is a small case series describing clinical presentations and does not test any treatment or cure.
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, dementia, and stem cell therapy
- Brain PET in the era of anti-amyloid-β antibody therapy for Alzheimer disease
- Improving the Bioavailability and Efficacy of Coenzyme Q10 on Alzheimer's Disease Through the Arginine Based Proniosomes
- Role of Microglia and Astrocytes in Alzheimer's Disease: From Neuroinflammation to Ca2+ Homeostasis Dysregulation
- Incidence and predictors of seizures in patients with Alzheimer's disease
- Safety and effectiveness of lecanemab in Chinese patients with early Alzheimer’s disease: Evidence from a multidimensional real-world study
- UCB Presents Data on Bepranemab (anti-tau antibody) in Early Alzheimer's Disease: Phase 2a TOGETHER Study
- Antioxidant vitamin intake and risk of Alzheimer disease
- Amyloid-β deposition in mild cognitive impairment is associated with increased hippocampal activity, atrophy and clinical progression
- Plasma lipid subspecies and Alzheimer’s disease: genetic evidence for risk and protection