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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In this study 5 patients with mild cognitive impairment (MCI) and 9 Alzheimer's disease (AD) patients underwent respectively 3- and 5-year follow-up positron emission tomography (PET) studies with N-methyl [(11)C] 2-(4-methylaminophenyl)-6-hydroxy-benzothiazole ((11)C-PIB) and (18)F-fluorodeoxyglucose ((18)F-FDG) to understand the time courses in AD disease processes.
Why it matters
In this small long-term PET study, amyloid retention increased in people with mild cognitive impairment and then stayed stable in clinical Alzheimer's disease, while brain glucose metabolism declined starting in mild cognitive impairment. This describes how imaging markers change over the disease course and does not test any treatment.
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Alzheimer disease (AD) is a heterogeneous and progressive neurodegenerative disease, which in Western society mainly accounts for senile dementia.
Why it matters
This review discusses inflammation, cytokines, immune response, APOE, cholesterol, and oxidative stress in Alzheimer disease and explores related therapeutic possibilities such as anti-inflammatory drugs, immunotherapy, diet, and curcumin. It is a review of hypotheses and does not provide evidence that any of these approaches prevents or cures the disease.
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The phosphatase and tensin homologue deleted on chromosome 10 (PTEN) negatively regulates intracellular levels of PIP3 and antagonizes the PI3K signaling pathway important for cell survival.
Why it matters
This study found that the protein PTEN was redistributed from the nucleus and cytoplasm to neurofibrillary tangles and other damaged structures in Alzheimer's disease brains, which the authors suggest may deregulate the PI3K pathway. It does not report any treatment, cure, or prevention of Alzheimer's disease.
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Amyloid precursor protein (APP) can be proteolytically processed along two pathways, the amyloidogenic that leads to the formation of the 40-42 amino acid long Alzheimer-associated amyloid β (Aβ) peptide and the non-amyloidogenic in which APP is cut in the middle of the Aβ domain thus precluding Aβ formation.
Why it matters
Amyloid-beta in spinal fluid is not only the familiar Aβ1-40 and Aβ1-42: this lab study used mass spectrometry to find "several shorter isoforms" as well. In a cell model built to mirror the spinal-fluid pattern, every isoform from Aβ1-17 upward depended on the enzyme γ-secretase, while shorter ones did not — pointing to a separate way these fragments are made. It is laboratory work on how amyloid is processed, not a test, treatment or prevention.
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Previous studies have described altered expression of metallothioneins (MTs) in neurodegenerative diseases like multiple sclerosis (MS), Down syndrome, and Alzheimer's disease (AD).
Why it matters
In three transgenic mouse models of Alzheimer disease amyloid deposits, MT-I mRNA was induced in all lines though the pattern differed, while MT-III mRNA expression was not significantly altered in any model. These animal findings suggest different metallothionein isoforms may have different roles in these models, but they do not establish any treatment, cure, or prevention for Alzheimer's disease.
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38/100
Affibody (Affibody) ligands specific for human amyloid beta (Abeta) peptides (40 or 42 amino acid residues in size), involved in the progress of Alzheimer's disease, were selected by phage display technology from a combinatorial protein library based on the 58-amino acid residue staphylococcal protein A-derived Z domain.
Why it matters
Researchers selected Affibody ligands that bind selectively to human amyloid-beta peptides in the laboratory. This is an early laboratory study and does not demonstrate any treatment, cure, or prevention for Alzheimer's disease.
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There are many who feel that the achievement of a disease-modifying (DM) designation for a drug is an important goal in Alzheimer disease (AD) therapeutics.
Why it matters
This is an opinion paper arguing that finding effective Alzheimer's drugs matters more than proving they are disease-modifying. It states that current methods for establishing disease modification have logistical and analytic problems and may fail even for truly effective drugs.
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The binding of amyloid beta peptides (Abeta) to plasma membranes appears to be a promising point of intervention in the events leading to the development of Alzheimer's disease (AD).
Why it matters
This review focuses on membrane proteins that can mediate the interaction between amyloid beta and the plasma membrane in Alzheimer's disease, including APP and the NMDA receptor. It discusses binding as a possible point of intervention but does not report a proven treatment, cure or prevention.
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Cerebral amyloid angiopathy (CAA) is a feature of ageing and Alzheimer's disease (AD); it is also associated with intracerebral hemorrhage and stroke.
Why it matters
This review describes how amyloid-beta becomes trapped in the drainage pathways along cerebral arteries in cerebral amyloid angiopathy, a feature of ageing and Alzheimer's disease. It evaluates possible effects of this on Alzheimer's therapies but reports no treatment or cure.
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Presenilin 1 (PS1) is a key factor for beta-amyloid (Ab) formation in Alzheimer disease (AD).
Why it matters
The study reports that S-adenosylmethionine administration silenced presenilin 1 in human neuroblastoma cells, which the authors suggest might prevent amyloid-beta formation. This is a cell-culture result and the proposed treatment idea is not established in patients.
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Despite important inroads into the molecular pathology of Alzheimer disease, effective long-term treatment for the condition remains elusive.
Why it matters
This review states that effective long-term treatment for Alzheimer disease remains elusive and that the roles apoE plays in the brain will be crucial to understanding the disease and developing therapies. It presents no new treatment, cure, or prevention findings.
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Despite the persistence of memory loss, the patients experienced a prompt and sustained response to mirtazapine.
Why it matters
This case summary describes three patients with dementia and depression complicated by weight loss, insomnia and anxiety who responded to mirtazapine. It is a small case report about symptom treatment, not a cure or prevention.
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The assessment of functional capacity is essential for the diagnosis of dementia by DSM-IV criteria and has important implications for patient intervention and management.
Why it matters
This study compared family members' judgments of functional abilities with objective measures in 72 patients diagnosed with Alzheimer's disease. It is about how caregivers rate daily function and does not test any treatment, cure, or prevention.
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Cerebral amyloid angiopathy (CAA) is the common term used to define the deposition of amyloid in the walls of medium- and small-size leptomeningeal and cortical arteries, arterioles and, less frequently, capillaries and veins.
Why it matters
This review discusses cerebral amyloid angiopathy, which is associated with Alzheimer disease and Down syndrome, and its relationship to stroke and dementia. It does not report any treatment or cure for Alzheimer disease.
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38/100
The apolipoprotein E genotype (APOE) is an established risk factor for Alzheimer disease, with the age-at-onset occurring earlier in individuals having at least one APOE epsilon 4 allele, relative to the APOE epsilon 3 or APOE epsilon 2 isoforms.
Why it matters
In this community sample of middle-aged adults, those with any APOE ε4 allele performed worse on learning and memory tasks than those with ε2 or ε3 genotypes. The authors suggest APOE may be a marker for age-related memory decline or for individual differences in memory ability.
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Three major lines of drugs have been developed or are under development for the treatment of Alzheimer Disease (AD): cholinergic drugs (mainly cholinesterase inhibitors), anti-beta-amyloid drugs, estrogens and anti-inflammatories.
Why it matters
This review states that cholinesterase inhibitors were the only drugs then approved for Alzheimer's disease and that several showed significant clinical efficacy and safety, mainly stabilizing cognitive function for six to 12 months. It also discusses future possibilities such as combining these drugs with estrogens, antioxidants and anti-inflammatories, and treating other dementias including Down syndrome dementia.
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Data from the Canadian Study of Health and Aging (CSHA) were used to examine the relation between severity of Alzheimer's disease, as measured by the Mini-Mental State Examination (MMSE), and costs of caring.
Why it matters
This study examined the link between Alzheimer's disease severity and the costs of caring for patients. It does not test any treatment, cure, or prevention for Alzheimer's disease.
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We completed a systematic survey of the human genome, conducted at an average resolution of 10 cM, for the identification of simple sequence tandem repeat polymorphisms (SSTRPs) that target new risk genes for Alzheimer disease (AD) by virtue of linkage disequilibrium.
Why it matters
This genome survey found six genetic markers associated with Alzheimer's disease, replicated in a separate sample, and suggests they may point to five new risk loci. One association appeared to come from linkage with the APOE epsilon 4 allele, and the others were not near previously known Alzheimer's risk genes.
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A consistent alteration in platelet APP isoforms has been found in Alzheimer disease and Down syndrome.
Why it matters
This study found a lower ratio of platelet amyloid precursor protein isoforms in patients with Alzheimer disease and in elderly patients with Down syndrome than in controls, while young patients with Down syndrome did not differ from controls. The authors say further studies are needed to know whether this could be a peripheral marker, so it is not a treatment or prevention finding.
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The frequency of the epsilon 4 allele of the apolipoprotein E (apoE) is increased in familial and sporadic late-onset Alzheimer's disease, but its prevalence in non-Alzheimer dementias in Caucasian populations is unknown.
Why it matters
This study found that the APOE ε4 allele was common not only in Alzheimer disease patients but also in those with vascular dementia and frontal-type dementia. The authors conclude that APOE ε4 is not unique to Alzheimer disease and its role as a risk factor should be reconsidered.
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38/100
A large number of familial Alzheimer disease (FAD) kindreds were examined to determine whether mutations in the amyloid precursor protein (APP) gene could be responsible for the disease.
Why it matters
This genetic study examined families with familial Alzheimer's disease for mutations in the APP gene, following earlier identification of three pathogenic mutations at codon 717. It looks at causes in rare inherited cases and reports no treatment or cure.
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37/100
Expert panels interpreted 1497 scans. Participants were a median age of 75 y (range, 65-96 y), 51.4% were female, and 60.5% had mild cognitive impairment.
Why it matters
In the IDEAS study, local clinical readers of amyloid PET scans agreed well with expert panel reads, with 86.6% agreement on positive scans and 91.5% on negative scans. This supports the reliability of amyloid PET reading in routine practice, but it is a diagnostic study and says nothing about treating, curing or preventing Alzheimer's disease.
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Mineralized blood vessels (MBV) are a form of vascular pathology associated with cerebrovascular aging and neurodegeneration; however, their regional distribution and clinicopathological correlates in Alzheimer disease (AD) remain poorly characterized.
Why it matters
Mineralized blood vessels were most frequent in the globus pallidus, followed by the posterior hippocampus and putamen, and were not associated with APOE ε4 carrier status or cerebral amyloid angiopathy. Mineralized blood vessels remained associated with état criblé in the putamen and globus pallidus.
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Lecanemab, an amyloid-targeting monoclonal antibody, was recently approved for early symptomatic Alzheimer's disease in South Korea.
Why it matters
In 112 Korean patients treated with lecanemab at one hospital, infusion-related reactions occurred in 37% and ARIA in 19% of those monitored, and demand outstripped infusion capacity with waits up to 20 weeks. This single-centre real-world experience describes safety and implementation challenges of an approved therapy, not a cure or prevention.
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We show that CD33M ectodomain dimerizes, enabling binding of large multi-sialylated molecules.
Why it matters
This laboratory work describes a mechanistic CLU:Aβ:CD33M axis and identifies CD33M dimerization and ligand-binding sites as potential therapeutic targets. These are structural, cellular, and genetic findings, and no treatment has been tested in patients.
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.
- Sex Differences in Longitudinal Tau-PET in Preclinical Alzheimer Disease: A Meta-Analysis
- Activated MAO-B in the brain of Alzheimer patients, demonstrated by [11C]-L-deprenyl using whole hemisphere autoradiography
- No effect of one-year treatment with indomethacin on Alzheimer's disease progression: a randomized controlled trial
- A pilot randomized trial of carbamazepine for behavioral symptoms in treatment-resistant outpatients with Alzheimer disease
- Future of Alzheimer's detection: Advancing diagnostic accuracy through the integration of qEEG and artificial intelligence
- Cerebrospinal Fluid Biomarkers for the Diagnosis of Alzheimer Disease in South Korea
- Caloric restriction attenuates Abeta-deposition in Alzheimer transgenic models
- Soluble TREM2 and Alzheimer-related biomarker trajectories in the blood of patients with diabetes based on their cognitive status
- Alzheimer's disease treated patients showed different patterns for oxidative stress and inflammation markers
- CSF Aβ42/Aβ40 and Aβ42/Aβ38 ratios: better diagnostic markers of Alzheimer disease