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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This study suggests that frontal executive deficits are present in half of ALS patients, many of whom meet strict research criteria for FTLD.
Why it matters
This study found that frontal executive deficits are present in half of ALS patients, many of whom meet criteria for frontotemporal lobar dementia. It concerns cognitive problems in ALS, not the treatment, cure or prevention of Alzheimer's disease.
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Sleep in the nursing home environment is extremely fragmented, possibly in part as a result of decreased light exposure.
Why it matters
This study found that morning and evening bright light led to more consolidated night-time sleep in patients with probable or possible Alzheimer's disease, and evening light improved circadian activity rhythm quality. It suggests nursing homes consider increasing ambient light, but reports no effect on curing or preventing the disease.
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This cross-sectional study examines relationships among the constellation of psychiatric syndromes in Alzheimer's disease (AD) as a function of dementia severity in 1155 patients with probable AD.
Why it matters
In 1,155 people with probable Alzheimer's disease, each seen once, major depression was less frequent in severe stages, while agitation, aggression and psychosis were more frequent in late stages. Symptoms tended to cluster: agitation went with aggression and psychosis, and depression went with sleep problems, anxiety and hopelessness at mild/moderate and severe stages. This snapshot describes patterns across different patients rather than changes in one person over time, and it tests no treatment.
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Alzheimer disease (AD) is the most common dementing illness in the elderly, but there is equivocal evidence regarding the frequency of other disorders such as Lewy body disease (LBD), vascular dementia (VaD), frontotemporal dementia (FTD), and hippocampal sclerosis (HS).
Why it matters
In 382 people with dementia whose brains were examined at the State of Florida Brain Bank, Alzheimer's disease was found in 77%, Lewy body disease in 26%, vascular dementia in 18%, hippocampal sclerosis in 13% and frontotemporal dementia in 5%. These overlap because many brains had more than one: Alzheimer's changes were also present in 66% of Lewy body, 77% of vascular and 66% of hippocampal sclerosis cases. Vascular dementia was relatively more common at older ages and frontotemporal and Lewy body disease less common. These are autopsy frequencies from one brain bank, not population rates or personal risk, and no treatment was tested.
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Recent epidemiological studies show a strong reduction in the incidence of Alzheimer's disease in patients treated with cholesterol-lowering statins.
Why it matters
In nerve cells grown in the lab, the cholesterol-lowering drugs simvastatin and lovastatin lowered levels of the amyloid-beta peptides Abeta42 and Abeta40; in guinea pigs given high doses of simvastatin, these levels fell in cerebrospinal fluid and brain and the fall was reversible. The authors propose that lower Abeta42 "may provide the mechanism" for the reduced dementia rates reported in statin users by earlier population studies, but this paper studied no people and measured no memory or dementia outcomes. These are laboratory and animal results that the authors say "may open up avenues for therapeutic interventions"; they do not show that statins prevent or treat Alzheimer's.
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Patients with AD and patients with FTD show different disturbances in their rhythms of activity and temperature compared with each other and with normal elderly patients.
Why it matters
This small study of 38 men found that people with Alzheimer's disease and people with frontotemporal degeneration had different patterns of disruption in their daily activity and body temperature rhythms. The findings are based on a small sample and do not test any treatment.
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We sought to determine the course of the preclinical episodic memory deficit in Alzheimer's disease.
Why it matters
This study found that people who later developed Alzheimer's disease already performed worse on word recall and recognition 3 and 6 years before diagnosis, while short-term memory was unaffected. It describes a long preclinical period of detectable episodic memory deficits, but reports no treatment or prevention.
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Citicoline has been extensively used for the treatment of neurodegenerative disorders associated with head trauma, stroke, brain aging, cerebrovascular pathology and Alzheimer's disease.
Why it matters
In this double-blind placebo-controlled study, citicoline improved cognitive performance in Alzheimer's disease patients who carried the APOE E4 allele, with more pronounced improvement in those with mild dementia. The study suggests citicoline might be useful, especially in certain patients, but it was a small trial and these findings need confirmation.
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Previous research has hypothesized an association between Alzheimer's disease and the amyloid precursor protein (APP) gene found on chromosome 21.
Why it matters
A 78-year-old woman with Down's syndrome who had only two copies of the APP gene showed no evidence of Alzheimer's disease on psychological, imaging and brain tissue tests. This single case supports the idea that having an extra copy of a region of chromosome 21 that includes APP is linked to Alzheimer's disease.
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Missense mutations in the presenilin 1 (PS1) gene cause the most common form of dominant early-onset familial Alzheimer's disease (FAD) and are associated with increased levels of amyloid beta-peptides (A beta) ending at residue 42 (A beta 42) in plasma and skin fibroblast media of gene carriers.
Why it matters
In four patients from a Colombian family with a presenilin 1 mutation, the study found increased A beta 42 deposition and severe cerebellar pathology. It describes how this inherited mutation causes early Alzheimer's pathology but does not provide a treatment, cure, or prevention.
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Homozygosity of the 1 allele in the PS-1 gene was associated with a doubling of the risk for late-onset Alzheimer's disease compared with the [12]/[22] genotype (odds ratio 1.97, 95% Cl 1.29-3.00).
Why it matters
This genetic study found that homozygosity for one allele in the presenilin-1 gene was associated with a doubling of the risk for late-onset Alzheimer's disease. The proportion of cases attributable to this locus was estimated at 0.22, compared with 0.35 for a single copy of APOE4.
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The protein beta-amyloid is said to be central to the disease process of Alzheimer's disease (AD).
Why it matters
This study analyzed beta-amyloid load in human brain tissue and its relation to dementia severity, noting that plaque numbers do not correlate well with cognition. It examines the role of amyloid in the disease process and does not test any treatment, cure or prevention.
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Alzheimer's disease (AD) is a central nervous system disorder characterized by the presence of neurofibrillary tangles, neuritic plaques and dystrophic neurones in susceptible areas of the brain.
Why it matters
This trial reported that idebenone was effective on memory, attention and orientation and slowed worsening in people with Alzheimer disease, with mild side effects. It is an older study of a symptomatic treatment, not a cure or prevention.
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54/100
Why it matters
Examines allelic variation in apolipoprotein E in sporadic Alzheimer's disease and the protein's interactions with receptors.
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Apolipoprotein E (apoE), a plasma apolipoprotein that plays a central role in lipoprotein metabolism, is localized in the senile plaques, congophilic angiopathy, and neurofibrillary tangles of Alzheimer disease.
Why it matters
This laboratory study found that both apolipoprotein E4 and E3 bind to the amyloid beta peptide, but E4 binds faster and behaves differently under varying acidity, which may help explain why the epsilon4 allele is linked to higher Alzheimer's risk. It is basic chemistry and does not test any treatment, cure or prevention.
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Why it matters
Reports a pathogenic mutation for probable Alzheimer's disease in the APP gene, at the N-terminus of β-amyloid.
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Why it matters
Discusses the molecular pathology of Alzheimer's disease.
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54/100
Ultrastructural studies of biopsied cortical tissue from the right frontal lobe of 8 patients with mild to moderate Alzheimer's disease (AD) revealed that the number of synapses in lamina III of Brodmann's area 9 was significantly decreased when compared with the number in age-matched control brains (n = 9; postmortem time, less than 13 hours).
Why it matters
Frontal lobe biopsies from 8 people with mild to moderate Alzheimer's had fewer synapses than control brains, and lower Mini-Mental State scores went with greater synapse loss. Remaining synapses were larger, which the authors see as the brain partly compensating, a capacity that was exceeded by end stage.
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Clinical and pathologic diagnoses are compared in 65 patients who had dementia and who had been studied longitudinally during life.
Why it matters
This study compared clinical and pathologic diagnoses in 65 patients with dementia, finding that the clinical diagnosis of dementia of the Alzheimer type had a sensitivity of 87% and specificity of 78%. It does not test a treatment or cure, but evaluates the accuracy of clinical diagnosis.
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A new rating instrument, the Alzheimer's Disease Assessment Scale, was designed specifically to evaluate the severity of cognitive and noncognitive behavioral dysfunctions characteristic of persons with Alzheimer's disease.
Why it matters
The Alzheimer's Disease Assessment Scale was designed specifically to evaluate the severity of cognitive and noncognitive behavioral dysfunctions characteristic of persons with Alzheimer's disease. In testing with 27 Alzheimer's disease subjects and 28 normal elderly subjects, those with Alzheimer's disease had significantly more cognitive and noncognitive dysfunction than the normal elderly subjects.
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Examination of temporal lobe structures from Alzheimer patients reveals a specific cellular pattern of pathology of the subiculum of the hippocampal formation and layers II and IV of the entorhinal cortex.
Why it matters
Examining temporal lobe tissue from Alzheimer patients, the authors found damage concentrated in specific cells of the hippocampal formation and entorhinal cortex that connect it with other brain structures crucial to memory. They suggest this pattern cuts the hippocampal formation off from much of its input and output and probably contributes to the memory disorder.
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Researchers isolated and purified a protein derived from twisted beta-pleated sheet fibrils in cerebrovascular amyloidosis associated with Alzheimer's disease using specific column chromatography and high performance liquid chromatography methods.
Why it matters
An initial report on purifying and characterising a cerebrovascular amyloid protein in Alzheimer's disease. Isolating and describing a protein is early laboratory groundwork that may open lines of research, not a treatment.
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This first evaluation of 18 F-MK6240 in DS demonstrates its suitability as a sensitive biomarker for Alzheimer's disease tau pathology.
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53/100
Moreover, there is limited knowledge regarding associations with domain-specific cognitive decline and modifying effects of key individual characteristics.
Why it matters
This prospective cohort study from the Swedish National Study on Aging and Care-Kungsholmen investigated whether blood biomarkers of Alzheimer's disease, including p-tau217, are associated with global and domain-specific cognitive decline. It addresses prediction of decline and does not test any treatment, cure, or prevention.
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P-tau217 demonstrated the most significant inter-group differences, the highest hazard ratio, and best distinguished MCI-Converters from MCI-Nonconverters, with its discriminative performance comparable to that of Aβ-PET measures and multi-plasma biomarker models.
Why it matters
This reanalysis of ADNI data found that plasma p-tau217 best distinguished people with MCI who converted to Alzheimer's dementia from those who did not, with performance comparable to amyloid PET. The findings support p-tau217 as a biomarker for predicting conversion from MCI to Alzheimer's dementia, but the study is about prediction, not treatment.
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.
- Plasma Biomarkers and Clinical Outcomes in Early-Onset Dementia
- Nonsteroidal anti-inflammatory drugs for the prevention of Alzheimer's disease: a systematic review
- Sleep quality and preclinical Alzheimer disease
- Neuronal expression of myeloperoxidase is increased in Alzheimer's disease
- Food combination and Alzheimer disease risk: a protective diet
- Elevated CSF levels of matrix metalloproteinase‐12 as a potential marker for microhemorrhage risk in autosomal dominant Alzheimer disease
- ApoE immunoreactivity and microglial cells in Alzheimer's disease brain
- Association of Insulin Resistance With Cerebral Glucose Uptake in Late Middle-Aged Adults at Risk for Alzheimer Disease
- Cloning of a gene bearing missense mutations in early-onset familial Alzheimer's disease
- Features of the Physical and Social Neighborhood Environment and Neighborhood-Level Alzheimer’s Disease and Related Dementia in South Carolina