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 5,413 studies, highest score first: BibTeX (.bib) · RIS (.ris)
Highest usefulness score first. Studies without a score come last.
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Older adults living in rural areas may face barriers to obtaining a diagnosis of Alzheimer's disease and related disorders (ADRD).
Why it matters
Using Medicare data on every beneficiary in Kentucky and West Virginia, this county-level study found that diagnosed Alzheimer's and related disorders were 11% less common in rural counties than urban ones in 2013 (95% CI: 9%–13%), after adjusting for age, sex, Medicaid eligibility and Appalachian location. The authors say this suggests rural older adults "may be underdiagnosed." It does not show that they have less dementia. Because the data are county averages, and some rural areas had younger, more male beneficiaries, the authors say individual-level studies are needed to confirm it.
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Alzheimer's disease (AD) is a complex age-related neurodegenerative disorder of the central nervous system.
Why it matters
This review reports that inflammatory pathways are activated in Alzheimer's disease brains and that people on long-term anti-inflammatory drugs have shown a reduced risk of developing the disease. It is a review of existing evidence, not a clinical trial, so it does not establish that anti-inflammatory drugs treat or prevent Alzheimer's.
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Down syndrome (DS) is one of the most common causes of intellectual disability, owing to trisomy of all or part of chromosome 21.
Why it matters
Proteomic analysis of frontal cortex found overlapping and independent molecular pathways contributing to Down syndrome, aging, and Alzheimer's pathology in Down syndrome. The authors say this may provide putative targets for therapeutic approaches, but no treatment was tested.
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Alzheimer disease (AD) is a complex neurodegenerative disorder, whose prevalence will dramatically rise by 2050.
Why it matters
This review notes that there is still no effective treatment for Alzheimer disease and that many trials produced negative or inconclusive results, possibly because they enrolled only patients with severe disease. It suggests that detecting and treating the disease in preclinical stages might be needed, but it reports no treatment that has been shown to work.
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Alzheimer´s disease (AD) is a neurodegenerative disorder with no known cure and rapid rise in incidence.
Why it matters
This review notes that Alzheimer's disease has no known cure and that current treatment mainly uses cognitive enhancers such as cholinesterase inhibitors. It describes molecular hallmarks and possible pathological mechanisms but reports no new treatment or preventive intervention.
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Apolipoprotein E (ApoE) polymorphism has been appreciated as a valuable predictor of Alzheimer disease (AD), and the associated ε4 allele has been recognized as an indicator of susceptibility to this disease.
Why it matters
Using two different detection methods, this study found significantly lower serum apolipoprotein E levels in Alzheimer's disease patients compared to controls. This is a biomarker finding and does not test any treatment, cure, or prevention.
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With the advent of the key discovery in the mid-1980s that the amyloid β-protein (Aβ) is the core constituent of the amyloid plaque pathology found in Alzheimer disease (AD), an intensive effort has been underway to attempt to mitigate its role in the hope of treating the disease.
Why it matters
This review describes efforts to target amyloid beta for treating Alzheimer's disease, including anti-Abeta aggregation inhibitors and immunization with Abeta that reduced pathology in animal models. It does not report a proven treatment or cure in people.
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Cerebrospinal fluid (CSF) samples from 33 patients with Alzheimer dementia (AD), 21 patients with mild cognitive impairment who converted to AD during followup (MCI-AD), 25 patients with stable mild cognitive impairment (MCI-stable), and 16 nondemented subjects (ND) were analyzed with a chemiluminescence immunoassay to assess the levels of the mitogen-activated protein kinase ERK1/2 (extracellular signal-regulated kinase 1/2).
Why it matters
This study found that a protein called ERK1/2 was higher in the spinal fluid of people with Alzheimer's dementia than in people with stable mild cognitive impairment or in people without dementia. However, as a diagnostic test for Alzheimer's, this protein was worse than the standard markers total tau, phosphorylated tau, and beta-amyloid 42.
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Hypercortisolemia and increased levels of hyperphosphorylated tau proteins in cerebrospinal fluid (CSF) are common features with pathogenic relevance in Alzheimer;s disease (AD).
Why it matters
In 26 patients with mild Alzheimer's dementia and 20 healthy controls, serum cortisol levels were inversely associated with cerebrospinal fluid tau markers. This small observational study does not show that changing cortisol levels treats or prevents Alzheimer's disease.
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Alzheimer's disease (AD) is the leading cause of dementia.
Why it matters
This study examined cerebrospinal fluid beta-amyloid 1-42 and total tau for diagnosing Alzheimer's disease in Tunisian patients and whether the APOE epsilon4 allele affected this. It is a diagnostic biomarker study, so it does not provide a treatment, cure or prevention.
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There is increasing evidence for blood-brain barrier (BBB) compromise in Alzheimer disease (AD).
Why it matters
This review examines how apolipoprotein E, amyloid-beta, and blood-brain barrier permeability are related in Alzheimer's disease. It notes that therapies targeting apoE/amyloid-beta and sealing a compromised blood-brain barrier are under development, but none are established treatments.
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Simple, non-invasive tests for an early detection of degenerative dementia by use of biomarkers are urgently required.
Why it matters
This paper describes a newly discovered gene and protein called ALZAS, expressed in brain regions and lymphocytes of Alzheimer's patients, and proposes it might become a simple blood test for early diagnosis. It is a proposal about a possible diagnostic marker, not evidence of any treatment, cure or prevention.
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Autism is characterized by restricted, repetitive behaviors and impairment in socialization and communication.
Why it matters
This study examined plasma neuronal proteins, secreted beta-amyloid precursor protein and amyloid-beta 40 and 42 peptides in children with and without autism. It is about autism, not Alzheimer's disease treatment, so it does not show how to treat, cure or prevent Alzheimer's disease.
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Alzheimer's disease, the most common neurodegenerative disorder of senile dementia, is characterized by two major morpho-pathological hallmarks.
Why it matters
This review describes basal forebrain cholinergic dysfunction in Alzheimer's disease and its suggested relationship to cognitive deficits, alongside amyloid, inflammation, and neurotrophin signaling. It summarizes mechanisms and does not establish any treatment, cure, or prevention.
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Region specific correlations between corpus callosum size and EEG coherence suggest that the decline in interhemispheric connectivity in Alzheimer's disease results from a specific loss of cortical association neurones projecting through the corpus callosum.
Why it matters
In this small study of 11 patients, corpus callosum size was reduced in Alzheimer's disease and correlated with interhemispheric EEG coherence. It is about understanding brain connectivity changes, not about a treatment, cure or prevention.
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Early diagnosis of Alzheimer s disease (AD) is relevant in order to initiate symptomatic treatment with antidementia drugs.
Why it matters
This review discusses whether CSF tau and beta-amyloid can help identify which people with mild cognitive impairment will progress to Alzheimer's. It is about improving early diagnosis, not about treating or preventing the disease.
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High-dose vitamin supplementation reduces homocysteine levels in patients with AD.
Why it matters
This small open-label study found that high-dose vitamins lowered homocysteine levels in people with Alzheimer's disease. It did not test whether this affects cognitive decline, so it does not show a treatment or prevention benefit.
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Cotton wool plaques (CWP) are large, ball-like plaques lacking dense amyloid cores that displace adjacent structures.
Why it matters
This describes a sporadic late-onset Alzheimer disease case with cotton wool plaques and compares it with 16 late-onset cases, finding that cotton wool plaques are not specific for early-onset familial disease. It is a pathology description and does not report a treatment, cure or prevention.
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Transgenic mice expressing in brain different mutant forms of the Amyloid Precursor Protein, develop functional, cognitive and pathological defects which resemble or are reminiscent of symptoms observed in Alzheimer's disease (AD) patients.
Why it matters
This paper describes transgenic mice that express mutant forms of the amyloid precursor protein and develop cognitive and pathological features resembling Alzheimer's disease. These animal models are useful for studying early biochemical and pathological aspects not accessible in human patients, and breeding them with other strains may help define how genetic factors interact, but this is animal research.
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Visual analogue scales may improve pain assessment in those AD patients who fully comprehend the meaning of the scales.
Why it matters
People in early and midstage Alzheimer's disease understood visual analogue pain scales less often than non-demented elderly people, and reported less intense pain and pain affect. This concerns how to assess pain in people with Alzheimer's disease, not how to treat, cure, or prevent it.
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Lesions of Alzheimer disease are associated with low-grade but sustained inflammatory responses.
Why it matters
This paper describes activated microglia clustering in the center of senile plaques and reactive astrocytes bordering amyloid beta deposits, with both cell types able to secrete inflammatory molecules. It is a descriptive account of inflammation in the Alzheimer's brain and tests no therapy.
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Alzheimer's disease is a common progressive neurodegenerative disease of unknown etiology.
Why it matters
This autopsy study found individual variation in the glutamate transporters GLAST and GLT but no significant correlation with Alzheimer's disease, except for a 14% lower ratio of N-terminal to central GLT immunoreactivity. It does not test any treatment, cure or prevention.
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In 1911, Alois Alzheimer published a detailed report (Zbl. ges.
Why it matters
Re-examination of Alois Alzheimer's 1911 case found numerous amyloid plaques but no neurofibrillary tangles, corresponding to a less common form of the disease. This is a historical and genetic analysis of one case and reports no treatment, cure or prevention.
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The distribution of apolipoprotein E (APOE) genotypes as a function of age and sex has been examined in a French population of 417 Alzheimer disease (AD) patients and 1,030 control subjects.
Why it matters
In this French population, the APOE ε4 allele was associated with increased Alzheimer disease risk compared with the ε3 allele, and risk estimates varied by age and sex. It is an observational genetic risk study and does not test any treatment, cure, or prevention.
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Alzheimer disease (AD) is accompanied by a marked loss of acetylcholinesterase (AChE) activity associated with cortical cholinergic axons and cholinoceptive neurons.
Why it matters
This study describes loss of acetylcholinesterase activity in Alzheimer's cortex alongside new cholinesterase activity associated with plaques, tangles and amyloid angiopathy, with different enzymatic properties. It is a description of pathology and reports no treatment, cure or prevention.
From across this topic
10 of the 5,374 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.
- Lecanemab use for early Alzheimer disease in Canada
- Differential memory test sensitivity for diagnosing amnestic mild cognitive impairment and predicting conversion to Alzheimer's disease
- Atherosclerosis, apolipoprotein E, and prevalence of dementia and Alzheimer's disease in the Rotterdam Study
- Benfotiamine and Cognitive Decline in Alzheimer's Disease: Results of a Randomized Placebo-Controlled Phase IIa Clinical Trial
- MiR-124 acts as a target for Alzheimer's disease by regulating BACE1
- Cerebral amyloid angiopathy burden associated with leukoaraiosis: a positron emission tomography/magnetic resonance imaging study
- Amyloid age and tau PET timeline to symptomatic Alzheimer’s disease in Down syndrome
- Consensus Recommendations for the Postmortem Diagnosis of Alzheimer’s Disease
- Imaging of amyloid beta in Alzheimer's disease with 18F-BAY94-9172, a novel PET tracer: proof of mechanism
- Decreased expression and activity of neprilysin in Alzheimer disease are associated with cerebral amyloid angiopathy