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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.

  1. The Alzheimer's Disease Neuroimaging Initiative

    ✓ Peer-reviewed alzhub usefulness score 54 out of 100. Neuroimaging Clinics of North America 2005-11-01 Long-term cohort studies

    This text describes the Alzheimer's Disease Neuroimaging Initiative, which addresses the growing incidence and socioeconomic impact of Alzheimer's disease as life expectancy increases.

    Why it matters

    Describes the Alzheimer's Disease Neuroimaging Initiative.

  2. Ways toward an early diagnosis in Alzheimer's disease: The Alzheimer's Disease Neuroimaging Initiative (ADNI)

    ✓ Peer-reviewed alzhub usefulness score 54 out of 100. Alzheimer s & Dementia 2005-07-01 Biomarkers

    With the increasing life expectancy in developed countries, the incidence of Alzheimer's disease (AD) and thus its socioeconomic impact are growing.

    Why it matters

    Argues that earlier and more accurate Alzheimer's diagnosis may come from combining imaging, spinal fluid and blood biomarkers. It describes the Alzheimer's Disease Neuroimaging Initiative (ADNI) as exploring which combinations work best for diagnosis and for tracking treatment effects.

  3. Brain glucose metabolism in the early and specific diagnosis of Alzheimer's disease. FDG-PET studies in MCI and AD

    ✓ Peer-reviewed alzhub usefulness score 54 out of 100. European journal of nuclear medicine and molecular imaging 2005-04-01 Getting a diagnosis

    The demographics of aging suggest a great need for the early diagnosis of dementia and the development of preventive strategies.

    Why it matters

    This review describes how FDG-PET imaging shows patterns of reduced brain glucose metabolism that can help identify Alzheimer's disease and predict future conversion, with about 90% sensitivity. It concerns diagnosis and prediction, not treating, curing or preventing Alzheimer's disease.

  4. Evaluation of the safety and immunogenicity of synthetic Abeta42 (AN1792) in patients with AD

    ✓ Peer-reviewed alzhub usefulness score 54 out of 100. Neurology 2005-01-01 Caregiving

    AN1792 + QS-21 elicited a positive antibody response to Abeta42 in more than half of this elderly study population.

    Why it matters

    In this phase 1 study, AN1792 produced an antibody response in some patients and Disability Assessment for Dementia scores showed less decline among treated patients than controls at week 84. Treatment-related adverse events occurred in some patients, and one patient developed meningoencephalitis diagnosed after death.

  5. Impact of APOE genotype on neuropathologic and neurochemical markers of Alzheimer disease

    ✓ Peer-reviewed alzhub usefulness score 54 out of 100. Neurology 2004-06-01 Genetics

    The epsilon4 allele does not predict cholinergic decline in AD.

    Why it matters

    In this autopsy series, carrying one APOE epsilon4 allele was not linked to most pathologic or neurochemical measures, though having two epsilon4 alleles was linked to more plaques and tangles. This describes how a risk gene relates to brain changes and does not offer a treatment or cure.

  6. Mild cognitive impairment: Can FDG-PET predict who is to rapidly convert to Alzheimer's disease?

    ✓ Peer-reviewed alzhub usefulness score 54 out of 100. Neurology 2003-04-22 Mild cognitive impairment

    Patients with mild cognitive impairment (MCI) were assessed, and a metabolic profile associated with conversion to AD at 18-month follow-up was sought.

    Why it matters

    Among patients with mild cognitive impairment, 7 who converted to Alzheimer's disease within 18 months had lower FDG PET glucose uptake in the right temporoparietal cortex than 10 who did not. The authors say FDG PET may identify rapid converters, pending replication.

  7. Are amyotrophic lateral sclerosis patients cognitively normal?

    ✓ Peer-reviewed alzhub usefulness score 54 out of 100. Neurology 2003-04-01 Getting a diagnosis

    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.

  8. Increased light exposure consolidates sleep and strengthens circadian rhythms in severe Alzheimer's disease patients

    ✓ Peer-reviewed alzhub usefulness score 54 out of 100. Behavioral sleep medicine 2003-01-01 Risk factors

    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.

  9. Psychiatric symptoms vary with the severity of dementia in probable Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 54 out of 100. The Journal of neuropsychiatry and clinical neurosciences 2003-01-01 Brain tissue and pathology

    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.

  10. Relative frequencies of Alzheimer disease, Lewy body, vascular and frontotemporal dementia, and hippocampal sclerosis in the State of Florida Brain Bank

    ✓ Peer-reviewed alzhub usefulness score 54 out of 100. Alzheimer disease and associated disorders 2002-10-01 Lewy body dementia

    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.

  11. Simvastatin strongly reduces levels of Alzheimer's disease beta -amyloid peptides Abeta 42 and Abeta 40 in vitro and in vivo

    ✓ Peer-reviewed alzhub usefulness score 54 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2001-04-10 How common it is

    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.

  12. Differential circadian rhythm disturbances in men with Alzheimer disease and frontotemporal degeneration

    ✓ Peer-reviewed alzhub usefulness score 54 out of 100. Archives of general psychiatry 2001-04-01 Caregiving

    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.

  13. Stability of the preclinical episodic memory deficit in Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 54 out of 100. Brain : a journal of neurology 2001-01-01 Getting a diagnosis

    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.

  14. Double-blind placebo-controlled study with citicoline in APOE genotyped Alzheimer's disease patients. Effects on cognitive performance, brain bioelectrical activity and cerebral perfusion

    ✓ Peer-reviewed alzhub usefulness score 54 out of 100. Methods and findings in experimental and clinical pharmacology 1999-11-01 Treatments

    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.

  15. Molecular mapping of Alzheimer-type dementia in Down's syndrome

    ✓ Peer-reviewed alzhub usefulness score 54 out of 100. Annals of neurology 1998-03-01 Risk genes beyond APOE

    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.

  16. The E280A presenilin 1 Alzheimer mutation produces increased A beta 42 deposition and severe cerebellar pathology

    ✓ Peer-reviewed alzhub usefulness score 54 out of 100. Nature medicine 1996-10-01 Risk genes beyond APOE

    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.

  17. Genetic association between intronic polymorphism in presenilin-1 gene and late-onset Alzheimer's disease. Alzheimer's Disease Collaborative Group

    ✓ Peer-reviewed alzhub usefulness score 54 out of 100. Lancet (London, England) 1996-02-01 Genetics

    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.

  18. Image analysis of beta-amyloid load in Alzheimer's disease and relation to dementia severity

    ✓ Peer-reviewed alzhub usefulness score 54 out of 100. Lancet (London, England) 1995-12-01 Cognitive tests and assessment

    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.

  19. Idebenone, a new drug in the treatment of cognitive impairment in patients with dementia of the Alzheimer type

    ✓ Peer-reviewed alzhub usefulness score 54 out of 100. Functional neurology 1994-05-01 Treatments

    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.

  20. Apolipoprotein E in sporadic Alzheimer's disease: Allelic variation and receptor interactions

    ✓ Peer-reviewed alzhub usefulness score 54 out of 100. Neuron 1993-10-01 Genetics

    Why it matters

    Examines allelic variation in apolipoprotein E in sporadic Alzheimer's disease and the protein's interactions with receptors.

  21. Binding of human apolipoprotein E to synthetic amyloid beta peptide: isoform-specific effects and implications for late-onset Alzheimer disease

    ✓ Peer-reviewed alzhub usefulness score 54 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1993-09-01 Genetics

    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.

  22. A pathogenic mutation for probable Alzheimer's disease in the APP gene at the N–terminus of β–amyloid

    ✓ Peer-reviewed alzhub usefulness score 54 out of 100. Nature Genetics 1992-08-01 Risk genes beyond APOE

    Why it matters

    Reports a pathogenic mutation for probable Alzheimer's disease in the APP gene, at the N-terminus of β-amyloid.

  23. The molecular pathology of Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 54 out of 100. Neuron 1991-04-01 Disease mechanisms

    Why it matters

    Discusses the molecular pathology of Alzheimer's disease.

  24. Synapse loss in frontal cortex biopsies in Alzheimer's disease: Correlation with cognitive severity

    ✓ Peer-reviewed alzhub usefulness score 54 out of 100. Annals of Neurology 1990-05-01 Brain tissue and pathology

    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.

  25. The Clinical Diagnosis of Alzheimer's Disease

    ✓ Peer-reviewed alzhub usefulness score 54 out of 100. Archives of Neurology 1987-01-01 Getting a diagnosis

    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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