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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The authors, a group of investigators with extensive research and clinical experience related to both late-life depression and Alzheimer disease (AD), propose provisional affective and behavioral inclusion and exclusion diagnostic criteria for Depression of AD.
Why it matters
This paper proposes provisional diagnostic criteria for depression of Alzheimer's disease. It is about diagnosis only and does not report any treatment, cure or prevention.
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Previous studies with positron-emission tomography (PET) and functional magnetic resonance imaging (fMRI) have indicated differences in neural metabolism and activity between carriers of the APOE epsilon4 allele and those who are not at risk for Alzheimer disease (AD).
Why it matters
This brain imaging study found no difference in activation patterns between people with and without the APOE epsilon 4 allele when doing difficult cognitive tasks. The authors conclude that the extra brain effort seen in people at genetic risk appears specific to memory encoding rather than to task difficulty in general.
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beta-Amyloid peptide (Abeta) is generated by two cleavages of amyloid precursor protein (APP).
Why it matters
This study measured mRNA levels of amyloid precursor protein forms, BACE, presenilin-1, and neprilysin across nine brain areas and several organs in Alzheimer's disease and control cases to estimate vulnerability to amyloid plaque formation. It is a descriptive comparison of gene expression and does not test any treatment, cure, or prevention.
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Both CSF tau and CSF phosphotau were increased in probable AD compared with FTD (p<0.001), SAE (p<0.001), PD (p<0.001), and controls (p<0.001).
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Mutations in the class I-like major histocompatibility complex gene called HFE are associated with hereditary hemochromatosis (HHC), a disorder of excessive iron uptake.
Why it matters
Screening DNA from people with familial Alzheimer's disease, adults with Down syndrome and healthy individuals for two hereditary hemochromatosis mutations, the study found that among people without the ApoE E4 allele, HFE mutations appeared to predispose to familial Alzheimer's disease in males but were somewhat protective in females. These findings are described as consistent with a proposition, not as a demonstrated cause or treatment.
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Apolipoprotein E (APOE) is the only confirmed susceptibility gene for late-onset Alzheimer disease (AD).
Why it matters
This genetic study found evidence for a possible second late-onset Alzheimer's risk locus on chromosome 12, in addition to the confirmed APOE gene. The results suggest that family size affects where the linkage signal is located, so the chromosome 12 findings remain uncertain.
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Atrophy of the hippocampal formation, a region important for the acquisition of new declarative knowledge, has been well-documented in Alzheimer's disease (AD), although the relation of such atrophy to the extent of memory dysfunction in these patients has been less clear.
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Senile plaques composed of A beta peptides are a histopathological hallmark of Alzheimer disease (AD).
Why it matters
This review explains that mutations in APP, PS1 and PS2 in early-onset familial Alzheimer's disease increase production of total amyloid beta or of amyloid beta ending at residue 42. It is a summary of disease mechanisms and reports no treatment, cure or prevention.
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Splice-site and missense mutations have been identified in tau associated with frontotemporal dementia with parkinsonism linked to chromosome 17.
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In this community-based cohort, subjects with severe AD were more likely to be hospitalized than unaffected subjects.
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43/100
Down syndrome is caused by over-expression of genes located within a segment of chromosome 21, termed the Down locus.
Why it matters
This review describes how overexpressed genes on chromosome 21, plus abnormal activity of genes elsewhere, are linked to Alzheimer-type brain degeneration in Down syndrome. It is a summary of molecular findings and does not report a treatment or cure.
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The preclinical stage of Alzheimer's disease is inconspicuous and there are - almost by definition - no reliable and valid symptoms and signs which would allow a very early diagnosis before the manifestation of irreversible deficits.
Why it matters
This paper describes the clinical features and stages of Alzheimer's disease, from preclinical to moderate dementia. It is a descriptive review and contains no treatment, cure or prevention findings.
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Microglial cells are considered to play an important role in the pathogenesis of Alzheimer disease.
Why it matters
In brain tissue from 20 people with Alzheimer's disease, the number of activated microglia and the area they occupied increased significantly with the number of APOE epsilon4 alleles. This postmortem study links APOE genotype to microglial activation but does not show that targeting microglia would treat or prevent the disease.
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Previous data from familial AD due to mutations in presenilin 1 and presenilin 2 genes and the amyloid precursor protein suggest that the long form of Abeta peptide, Abeta42, is selectively increased in these circumstances.
Why it matters
Examining temporal lobe brain tissue from 28 people with Alzheimer's, researchers found that carrying two copies of the APOE epsilon4 risk gene was associated with more Abeta40 deposits. The pattern differed from that seen in Alzheimer's caused by presenilin 1, presenilin 2 or amyloid precursor protein mutations. The authors suggest APOE epsilon4 raises amyloid buildup through a different mechanism than these other genetic causes, which helps explain disease biology rather than offering a therapy.
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Mutations in the human presenilin genes (PSEN1 and PSEN2) are associated with early onset familial Alzheimer disease.
Why it matters
This study analyzed the 5' sequence, genomic structure and alternative splicing of the presenilin-1 gene associated with early-onset Alzheimer's disease. It is a gene structure analysis and does not test any treatment, cure or prevention.
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Dementia with brainstem and neocortical Lewy bodies (LB) is a source of ongoing nosologic controversy and confusion.
Why it matters
This brain autopsy study shows that how often dementia with Lewy bodies is classified as mixed with Alzheimer's disease versus pure Lewy body disease depends heavily on which Alzheimer's diagnostic criteria are used. It is about how dementia is defined and classified, not about treating, curing, or preventing it.
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Late-onset Alzheimer disease (AD) is associated with the apolipoprotein E (APOE)-epsilon4 allele.
Why it matters
In families with late-onset Alzheimer's disease, women with one APOE epsilon4 allele had about twice the risk of men with the same genotype. This helps explain why women may be more affected but does not provide a way to treat, cure or prevent the disease.
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Apolipoprotein-E epsilon 4 (APOE-epsilon 4) has been consistently associated with Alzheimer disease (AD) and may be responsible for an earlier age at onset.
Why it matters
Having two copies of the APOE-ε4 allele raised the relative risk of Alzheimer's disease in African American, Caucasian, and Hispanic groups. One copy of APOE-ε4 raised risk in Caucasians and Hispanics but not in African Americans, showing the genetic risk differs by ethnic group.
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The complement protein, C1q, has been shown to bind to fibrillar beta-amyloid, resulting in the activation of the classical complement pathway.
Why it matters
This study found that the complement protein C1q colocalized with nearly all thioflavine-positive plaques in Alzheimer's disease brain. It reports no treatment, cure, or prevention.
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This study examines the relationship between the levels of apolipoprotein E (apoE) and apolipoprotein J (apoJ, also designated as clusterin) as a function of apoE genotype in the hippocampus and cortex of Alzheimer disease (AD) subjects.
Why it matters
In hippocampus and frontal cortex tissue from Alzheimer's disease subjects, apolipoprotein E levels were reduced in proportion to the number of APOE ε4 alleles, while apolipoprotein J (clusterin) levels increased proportionately. This suggests a possible compensatory response in the brain, but it is tissue-level research and does not show a treatment, cure, or prevention.
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A peptide corresponding to the amino acid sequence of A beta 17-42 (LVFFAEDVGSNKGAIIGLMVGGVVIA) was isolated from Alzheimer Disease patient brains containing large deposits of diffuse-type amyloid.
Why it matters
This chemical study isolated and identified a specific amyloid beta fragment, Aβ17-42, from the brains of Alzheimer's disease patients who had large amounts of diffuse amyloid deposits. It describes the composition of these deposits but provides no information about treating, curing, or preventing the disease.
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beta-Amyloid formation requires multiple abnormal proteolytic cleavages of amyloid precursor protein (APP), including one within its intramembrane domain.
Why it matters
In brain tissue from people with Alzheimer's disease, lysosomal hydrolases were abnormally distributed compared with controls. This describes a difference in tissue and does not show that changing lysosomal function treats or prevents the disease.
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Alzheimer senile plaques are comprised of extracellular deposits of beta-amyloid.
Why it matters
This ultrastructural study found amyloid fibrils closely interdigitated with cells identified morphologically as microglia, the brain's resident macrophages. It is a descriptive tissue study and tests no treatment, cure or prevention.
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Glial fibrillary acidic protein (GFAP), a protein that is associated with 9-nm filaments of astrocytes, was observed to be increased in the astrocytes surrounding senile plaques in patients with Alzheimer dementia and in aged subjects without dementia.
Why it matters
GFAP was found to be increased in astrocytes surrounding senile plaques in people with Alzheimer dementia and in aged subjects without dementia. This is an observation about brain tissue and reports no treatment, cure or prevention.
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Alzheimer disease was transmitted in a pattern consistent with an autosomal dominant trait in three families.
Why it matters
This older study reported Alzheimer disease transmitted in an autosomal dominant pattern in three families and noted associations with abnormal neurofibrillary structures, Down syndrome, and aneuploidy. It is a descriptive family and tissue observation that offers 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.
- ReIU: an efficient preliminary framework for Alzheimer patients based on multi-model data
- Alzheimer's disease - a neurospirochetosis. Analysis of the evidence following Koch's and Hill's criteria
- Clinical progression on CDR‐SB©: Progression‐free time at each 0.5 unit level in dominantly inherited and sporadic Alzheimer's disease populations
- Multitarget Compounds Designed for Alzheimer, Parkinson, and Huntington Neurodegeneration Diseases
- Neuropsychiatric symptoms as a predictor of caregiver burden in Alzheimer's disease
- Investigating Heterogeneity and Neuroanatomic Correlates of Longitudinal Clinical Decline in Atypical Alzheimer Disease
- Reconsidering harbingers of dementia: progression of parietal lobe white matter hyperintensities predicts Alzheimer's disease incidence
- Clinical Meaningfulness of Donanemab in Early Symptomatic Alzheimer Disease: Data From the Randomized Phase 3 TRAILBLAZER-ALZ 2 Trial
- Adaptive, dose-finding phase 2 trial evaluating the safety and efficacy of ABT-089 in mild to moderate Alzheimer disease
- Imaging markers for Alzheimer disease: which vs how