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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These results suggest that BD is associated with decreased volumes of medial temporal lobe structures, with greater effect sizes in the amygdala than in the hippocampus.
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Amyloid deposition can take place in the walls of arteries, arterioles, and, less often, capillaries and veins of the central nervous system, a phenomenon known as cerebral amyloid angiopathy (CAA).
Why it matters
This review describes cerebral amyloid angiopathy, in which amyloid deposits in blood vessel walls can cause cerebral hemorrhage, ischemic lesions and dementia, and notes that it can be severe in some familial forms of Alzheimer's disease. It explains disease mechanisms and does not test any treatment or prevention.
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Epidemiological studies found associations between hyperhomocysteinaemia and both histologically confirmed AD and disease progression and revealed that dementia in AD was associated with evidence of brain infarcts on autopsy.
Why it matters
This review reports that high homocysteine levels were found to be a strong, independent risk factor for dementia and Alzheimer's disease, and that homocysteine falls when B-group vitamin status rises. It raises the hope that mental decline or Alzheimer's disease could be prevented by dietary modification or food fortification, but this is not yet proven.
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Vaccination against human beta-amyloid peptide (A beta) has been shown to remove the amyloid burden produced in transgenic mice overexpressing the mutated human amyloid precursor protein (APP) gene.
Why it matters
Mouse studies had shown that vaccination against beta-amyloid could clear amyloid, but this study asked whether human amyloid looks the same. Using mass spectrometry on post-mortem brain tissue, the researchers found that amino-truncated (shortened) forms made up "more than 60% of all A beta species", both in full Alzheimer's disease and in people without dementia who had only the earliest brain changes. This is laboratory work on brain tissue; it did not test a vaccine and does not show that vaccination works in people.
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Neither dietary, supplemental, nor total intake of carotenes and vitamins C and E was associated with a decreased risk of AD in this study.
Why it matters
In this cohort of 980 elderly people followed for a mean of 4 years, intake of carotenes, vitamin C, or vitamin E in dietary or supplemental form was not associated with a decreased risk of Alzheimer disease. The study found no protective effect for these antioxidant vitamins.
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Heterozygous APP23 mice, expressing human amyloid-precursor protein with the Swedish double mutation and control littermates, were subjected to behavioral and neuromotor tasks at the age of 6-8 weeks, 3 and 6 months.
Why it matters
In the APP23 mouse model, age-dependent cognitive decline appeared before amyloid deposition, with major learning and memory deficits from 3 months of age. This is animal research and does not test a treatment or cure for people.
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Reductions in cholinergic function occur in Alzheimer disease (AD) and dementia with Lewy bodies and correlate with cognitive decline.
Why it matters
This autopsy study examined the timing of cholinergic deficits in 89 patients with Alzheimer's disease and 50 with the Lewy body variant of Alzheimer's disease. It describes brain changes by disease stage and does not test any treatment, cure, or prevention.
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Cerebral amyloid angiopathy (CAA) is a type of beta-amyloidosis that occurs in leptomeningeal and cortical vessels of the elderly.
Why it matters
This study of brain tissue described two types of sporadic cerebral amyloid angiopathy, differing by whether amyloid was present in cortical capillaries. The APOE epsilon 4 allele was more common in one type and the epsilon 2 allele more common in the other, suggesting they are distinct conditions.
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Different patterns of regional brain atrophy were found among patients of different APOE genotypes.
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Immunization with preaggregated amyloid beta-peptide (Abeta(1-42)) and administration of antibodies against Abeta into amyloid precursor protein APP(V717F)- transgenic mice (an animal model of AD) have recently been reported to dramatically reduce amyloid plaque deposition, neuritic dystrophy, and astrogliosis, most likely by enhancing Abeta clearance from brain.
Why it matters
Using a sensitive ELISA, this study found reduced levels of naturally occurring anti-beta-amyloid antibodies in the cerebrospinal fluid of Alzheimer's disease patients compared with age-matched controls. It is an observational measurement and does not show that giving such antibodies treats the disease in people.
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47/100
Why it matters
An MRI study of atrophy in the entorhinal cortex and hippocampus in incipient and very mild Alzheimer's disease.
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FE65 binds to the Alzheimer amyloid precursor protein (APP), but the function of this interaction has not been identified.
Why it matters
This laboratory study found that APP and FE65 proteins help regulate cell movement and that overexpressing APP speeds up cell migration in a wound-healing assay. It does not test any treatment, cure, or prevention of Alzheimer's disease in people.
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We demonstrate that phonological and articulatory impairments may occur at presentation or early in the course of Alzheimer's disease, contrary to claims that these aspects of language production are relatively preserved until the final stages of this disease.
Why it matters
In six patients with pathologically confirmed Alzheimer's disease and four with clinically diagnosed dementia of the Alzheimer's type, analysis of speech revealed false start errors, phonological paraphasias and articulatory difficulty, contrary to the claim that these aspects of language production are preserved until late stages. This is a small case series describing symptoms and does not test treating, curing or preventing Alzheimer's disease.
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Antibodies to alpha-synuclein (AS) now provide a sensitive and specific method for the detection of Lewy bodies (LBs) and their use will allow a more accurate determination of the prevalence of LBs in Alzheimer's Disease (AD).
Why it matters
Using alpha-synuclein staining on brain tissue from 145 people with sporadic Alzheimer's disease, the study found Lewy bodies in 88 of them (60.7%). In every case with Lewy bodies the amygdala was involved and had the most of them.
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Our findings add to the preexisting literature because we tested alternative models of caregiver burden using an unusually large sample size of participants and after overcoming methodological limitations of past research.
Why it matters
In 613 Canadian families caring for someone with dementia, caregivers felt more burdened when the person had more disturbing behaviors, lived at home rather than in an institution, or when family and friends gave little help — and that sense of burden went along with more depressive symptoms. Caregivers of people with more disturbing behaviors and functional limitations actually received less help from family and friends. The authors suggest managing difficult behaviors, offering formal services to caregivers who lack informal support, and building coping skills, though the study itself tested associations, not these interventions.
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Clinical differential diagnosis of early-onset dementia (EOD) includes familial Alzheimer disease (FAD) and hereditary prion disease.
Why it matters
Screening four genes in patients with early-onset dementia found a high prevalence of pathogenic mutations in presenilin, amyloid precursor protein, and prion protein genes. This is a diagnostic and genetic finding and does not provide a treatment, cure, or prevention for Alzheimer's disease.
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These findings indicate that the use of antipsychotic agents and sedatives can affect the natural course of Alzheimer disease.
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Amyloid deposition is a neuropathological hallmark of Alzheimer's disease.
Why it matters
In rats, the amyloid precursor protein is transported along axons to nerve terminals, where it may be processed into amyloid beta. This describes a possible site of amyloid formation but tests no treatment and shows no effect on disease.
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47/100
'Amygdala' and 'amygdalar complex' are terms that now refer to a highly differentiated region near the temporal pole of the mammalian cerebral hemisphere.
Why it matters
This paper argues that the amygdala is not a single structural or functional unit but a set of cell groups belonging to several functional systems. It is a basic anatomy paper with no findings on treating, curing or preventing Alzheimer's disease.
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Brain imaging techniques have the potential to characterize neurobiological changes that precede the onset of cognitive impairment in persons at risk for Alzheimer's disease.
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In light of recent reports of diminished platelet serotonin concentration and increased plasma serotonin levels in patients with Alzheimer disease (AD), we hypothesized that a state of heightened platelet activation might be present in AD.
Why it matters
In 91 people with probable Alzheimer's and 40 age-matched controls, blood from the Alzheimer's group showed more signs of activated platelets: 39.5% more platelet clumps, 59.3% more of the activation marker CD62p, and 53.3% more white-cell–platelet complexes. Routine measures such as platelet count and fibrinogen did not differ. This is a single snapshot comparison that suggests a possible blood marker; it does not show cause, test any treatment, or give a test usable for individuals.
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A variety of anatomic and functional neuroimaging findings are associated with Alzheimer's disease (AD).
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The most common cause of dementia occurring in mid- to late-life is Alzheimer's disease (AD).
Why it matters
This review discusses mutant genes in familial Alzheimer's disease, including those encoding amyloid precursor protein and presenilins. These mutant gene products cause dysfunction or death of vulnerable populations of nerve cells important in memory, higher cognitive processes, and behavior.
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Many approaches have been undertaken to understand Alzheimer's disease (AD) but the heterogeneity of the etiologic factors makes it difficult to define the clinically most important factor determining the onset and progression of the disease.
Why it matters
This paper proposes that disturbed glucose metabolism, oxidative stress and advanced glycation endproducts interact in a vicious cycle that contributes to the onset and progression of Alzheimer's disease. It is a review of evidence rather than a clinical trial, so it does not show that targeting these factors treats or prevents the disease.
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In Reply. —The analyses of Drs Mirra and Gearing indicate that brain infarcts are not associated with NFTs in the neocortex.
Why it matters
In this reply letter, the authors report that brain infarcts were not associated with the number of tangles or plaques in the neocortex, suggesting the two occur independently. Among participants who met their criteria for Alzheimer's, dementia prevalence was 93% in those with subcortical lacunar infarcts and 57% in those without.
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.
- Multi-dimensional attention framework for personalised Alzheimer's disease progression prediction across sporadic and genetic risk cohorts
- Amyloid beta(1-42) and phosphorylated tau in CSF as markers for early-onset Alzheimer disease
- Vascular endothelial-cadherin as a marker of endothelial injury in preclinical Alzheimer disease
- Plasma Biomarker Characterization of Alzheimer’s Disease Psychosis in Study ACP‐204‐006
- Dynamic changes in plasma biomarkers of Alzheimer's disease in patients treated with lecanemab: a longitudinal cohort study
- Effect of acupuncture in mild cognitive impairment and Alzheimer disease: a functional MRI study
- Apolipoprotein E in Alzheimer's disease and other neurological disorders
- Optical Coherence Tomography in Alzheimer's Disease: A Meta-Analysis
- Conversion of amnestic Mild Cognitive Impairment to dementia of Alzheimer type is independent to memory deterioration
- Changes in brain functional connectivity in Alzheimer-type and multi-infarct dementia