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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.

Highest usefulness score first. Studies without a score come last.

  1. PET imaging of amyloid in Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 50 out of 100. The Lancet. Neurology 2004-09-01 Getting a diagnosis

    Alzheimer's disease (AD) is the most common form of dementia and is characterised by progressive impairment in cognitive function and behaviour.

    Why it matters

    This 2004 review surveys three ways researchers were trying to see amyloid plaques in the living brain: antibodies, which had "limited uptake by the brain"; an MRI agent, tested only in mice; and small-molecule tracers, which it calls the most successful approach so far. It reports that two PET tracers, FDDNP and PIB, "show more binding in the brains of patients with AD than in those of healthy people", but gives no accuracy figures. Its case for amyloid imaging is a hoped-for one, early diagnosis and judging new treatments, not a tested diagnostic or treatment result.

  2. Reduced risk of Alzheimer disease in users of antioxidant vitamin supplements: the Cache County Study

    ✓ Peer-reviewed alzhub usefulness score 50 out of 100. Archives of neurology 2004-01-01 Prevention and risk

    Use of vitamin E and vitamin C supplements in combination is associated with reduced prevalence and incidence of AD.

    Why it matters

    In this study, combined use of vitamin E and C supplements was associated with reduced prevalence and incidence of Alzheimer disease. No evidence of a protective effect was seen with use of vitamin E or vitamin C supplements alone, or with multivitamins alone.

  3. Alzheimer's disease and the basal forebrain cholinergic system: relations to beta-amyloid peptides, cognition, and treatment strategies

    ✓ Peer-reviewed alzhub usefulness score 50 out of 100. Progress in neurobiology 2002-10-01 Brain tissue and pathology

    Alzheimer's disease (AD) is the most common form of degenerative dementia and is characterized by progressive impairment in cognitive function during mid- to late-adult life.

    Why it matters

    This review presents evidence implicating the basal forebrain cholinergic system in Alzheimer's disease pathogenesis and its accompanying cognitive deficits. It discusses the relationship between beta-amyloid peptides, cognition, and treatment strategies targeting this system.

  4. Lipid peroxidation in aging brain and Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 50 out of 100. Free radical biology & medicine 2002-09-01 Getting a diagnosis

    Lipid peroxidation is one of the major outcomes of free radical-mediated injury that directly damages membranes and generates a number of secondary products, both from fission and endocyclization of oxygenated fatty acids that possess neurotoxic activity.

    Why it matters

    This 2002 review pulls together studies showing more lipid peroxidation (oxidative damage to cell membranes, mostly in neurons) in Alzheimer's brains than in age-matched controls, and says this damage is "not a significant feature of usual aging." It points to cerebrospinal-fluid isoprostanes as a possible lab marker: raised early in the dementia in a few studies, with one study suggesting better diagnostic accuracy. It also reports that blood and urine measurements were inconsistent. It tests no treatment, so it does not show that antioxidants or any other therapy help.

  5. Cholinesterase inhibitor treatment alters the natural history of Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 50 out of 100. Journal of neurology, neurosurgery, and psychiatry 2002-03-01 Treatments

    The short and long term effects of CEIs were evaluated in 135 patients with probable Alzheimer's disease relative to 135 patients who were never exposed to CEIs matched by age, education, duration of the symptoms, and cognitive status.

    Why it matters

    This study compared 135 Alzheimer's patients taking cholinesterase inhibitors with 135 matched patients never exposed to them, measuring cognitive and functional change and outcomes such as nursing home admission and death over about three years. It examined whether these existing drugs alter the course of the disease, not whether they cure or prevent it.

  6. New frontiers in Alzheimer's disease genetics

    ✓ Peer-reviewed alzhub usefulness score 50 out of 100. Neuron 2001-10-01 Risk genes beyond APOE

    Alzheimer's disease (AD) is a genetically complex disorder that accounts for the majority of dementia in the elderly population.

    Why it matters

    This review states that over 100 rare mutations in three genes cause early-onset familial Alzheimer's disease, that a polymorphism in the apolipoprotein E gene is associated with increased susceptibility to late-onset disease, and that these four genes account for less than 30% of the genetic variance. It summarizes genetic knowledge but does not report a treatment, cure, or prevention.

  7. Incidence of Alzheimer's disease in a rural community in India: the Indo-US study

    ✓ Peer-reviewed alzhub usefulness score 50 out of 100. Neurology 2001-09-01 Disparities

    These are the first AD incidence rates to be reported from the Indian subcontinent, and they appear to be among the lowest ever reported.

    Why it matters

    The first Alzheimer's incidence figures reported from the Indian subcontinent: in rural Ballabgarh, about 4.7 new cases per 1,000 people aged 65+ per year (age-adjusted), against 17.5 in a Pennsylvania comparison community. The authors call these "among the lowest ever reported" but warn that the short 2-year follow-up, "cultural factors, and other potential confounders" mean the gap should be read with caution. It shows how often the disease appeared in two places; it does not show why, and tests no treatment or prevention.

  8. Early detection and differential diagnosis of Alzheimer's disease and depression with neuropsychological tasks

    ✓ Peer-reviewed alzhub usefulness score 50 out of 100. Dementia and geriatric cognitive disorders 2001-07-01 Getting a diagnosis

    The development of novel treatments for Alzheimer's disease (AD), aimed at ameliorating symptoms and modifying disease processes, increases the need for early diagnosis.

    Why it matters

    In 26 people with mild Alzheimer's disease, 43 with questionable dementia, 37 with major depression and 39 healthy controls, a visuo-spatial associative learning test distinguished Alzheimer's disease from depressed and control subjects. This is a small diagnostic study and provides no information on treating, curing or preventing Alzheimer's disease.

  9. Mild cognitive impairment and Alzheimer disease: regional diffusivity of water

    ✓ Peer-reviewed alzhub usefulness score 50 out of 100. Radiology 2001-04-01 Mild cognitive impairment

    Hippocampal ADC was significantly different between control subjects and MCI patients, many of whom likely have preclinical Alzheimer disease.

    Why it matters

    Hippocampal apparent diffusion coefficient was higher in people with mild cognitive impairment and Alzheimer's disease than in controls, while anisotropy index showed no differences among groups except in the occipital region. The authors suggest elevated hippocampal ADC may reflect early ultrastructural changes in Alzheimer's disease progression.

  10. Extended-release physostigmine in Alzheimer disease: a multicenter, double-blind, 12-week study with dose enrichment. Physostigmine Study Group

    ✓ Peer-reviewed alzhub usefulness score 50 out of 100. Archives of general psychiatry 2000-02-01 Treatments

    Physostigmine demonstrated a statistically significant benefit compared with placebo on a clinical global rating of change and an objective test of cognitive function.

    Why it matters

    Extended-release physostigmine scored better than placebo on two cognitive and global measures in people with mild-to-moderate Alzheimer disease, but showed no significant improvement on another global measure or secondary outcomes. Nausea and vomiting were common side effects.

  11. Delusions and hallucinations in Alzheimer's disease: prevalence and clinical correlates

    ✓ Peer-reviewed alzhub usefulness score 50 out of 100. International journal of geriatric psychiatry 2000-02-01 Clinical safety

    This study confirms the high prevalence of psychotic symptoms in AD patients encountered in clinical practice and suggests that individual psychotic symptoms have different associations.

  12. Cerebral infarcts in patients with autopsy-proven Alzheimer's disease: CERAD, part XVIII. Consortium to Establish a Registry for Alzheimer's Disease

    ✓ Peer-reviewed alzhub usefulness score 50 out of 100. Neurology 1998-07-01 Cognitive tests and assessment

    Prior studies report that subjects with neuropathologic evidence of AD and concomitant brain infarcts had poorer cognitive function and higher frequency of dementia than those with AD alone.

    Why it matters

    Among people whose Alzheimer's was confirmed at autopsy, the 32 who also had brain infarcts or lacunar lesions were older at death than the 74 with Alzheimer's alone, and their dementia was more severe at the final visit. The findings tie added vascular brain damage to more severe dementia in Alzheimer's, although the patients with both were also older.

  13. Estimation of the genetic contribution of presenilin-1 and -2 mutations in a population-based study of presenile Alzheimer disease

    ✓ Peer-reviewed alzhub usefulness score 50 out of 100. Human molecular genetics 1998-01-01 Risk genes beyond APOE

    Two closely related genes, the presenilins ( PS ), located at chromosomes 14q24.3 and 1q42.1, have been identified for autosomal dominant Alzheimer disease (AD) with onset age below 65 years (presenile AD).

    Why it matters

    Researchers screened both presenilin genes (PS-1 and PS-2) in 101 unrelated people with Alzheimer's that began before age 65, drawn from a population-based series in which APP gene mutations had already been ruled out. They found four different PS-1 mutations in six people, all from familial cases (two from families with a clear dominant inheritance pattern). The study measures how often these genes are involved in early-onset disease; it does not apply to typical late-onset Alzheimer's and offers no treatment.

  14. Microglial activation by Alzheimer amyloid precursor protein and modulation by apolipoprotein E

    ✓ Peer-reviewed alzhub usefulness score 50 out of 100. Nature 1997-08-01 Risk genes beyond APOE

    A role for beta-amyloid precursor protein (beta-APP) in the development of Alzheimer's disease has been indicated by genetics, and many conditions in which beta-APP is raised have been associated with an increased risk of Alzheimer's disease or an Alzheimer's-like pathology.

    Why it matters

    In laboratory experiments, a secreted fragment of APP activated microglia and increased their production of neurotoxins, and this was blocked by apolipoprotein E3 but not E4. This suggests a possible link between APP, inflammation, and apolipoprotein E, but it is early laboratory work and no treatment was tested.

  15. Apolipoprotein E and Alzheimer disease

    ✓ Peer-reviewed alzhub usefulness score 50 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1995-05-01 Genetics

    Inheritance of specific apolipoprotein E (apoE) alleles determines, in large part, the risk and mean age of onset of late-onset familial and sporadic Alzheimer disease.

    Why it matters

    This review explains that inheriting specific apolipoprotein E alleles largely determines the risk and mean age of onset of late-onset Alzheimer disease, but the mechanism by which the apoE isoforms differentially contribute to disease expression is unknown. It describes isoform-specific interactions of apoE with tau and amyloid beta that give rise to testable hypotheses, but no treatment, cure, or prevention is established.

  16. Extrapyramidal signs and psychiatric symptoms predict faster cognitive decline in Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 50 out of 100. Archives of neurology 1994-07-01 Cognitive tests and assessment

    A cohort of patients was followed up longitudinally and the likelihood of arriving at two cognitive end points was assessed using the Cox proportional hazards model and eight explanatory variables.

    Why it matters

    This cohort study followed 135 patients with Alzheimer's disease to identify clinical predictors of faster cognitive decline. It describes which symptoms predict decline and does not test any treatment, cure, or prevention.

  17. Detection of an Alzheimer disease pattern of cerebral metabolism in Down syndrome

    ✓ Peer-reviewed alzhub usefulness score 50 out of 100. Dementia (Basel, Switzerland) 1994-03-01 Down syndrome and Alzheimer's

    Correlational analysis of cerebral metabolic (rCMRglc) data obtained with positron emission tomography (PET) assesses group differences and has demonstrated reduced frontal-parietal rCMRglc interdependencies in Alzheimer's disease (AD).

    Why it matters

    Discriminant functions based on cerebral metabolic data classified all Down syndrome adults with dementia and some without dementia as having an Alzheimer's disease pattern. The authors suggest utility for early detection, which is about diagnosis rather than treatment or cure.

  18. Temporal lobe regions on magnetic resonance imaging identify patients with early Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 50 out of 100. Archives of neurology 1993-09-01 Vascular contributions

    The results suggest that the hippocampus and the temporal horn of the lateral ventricles may be useful as antemortem markers of AD in mildly impaired patients.

  19. Mitochondrial DNA variants observed in Alzheimer disease and Parkinson disease patients

    ✓ Peer-reviewed alzhub usefulness score 50 out of 100. Genomics 1993-07-01 Brain tissue and pathology

    Mitochondrial DNA (mtDNA) variants associated with Alzheimer disease (AD) and Parkinson disease (PD) were sought by restriction endonuclease analysis in a cohort of 71 late-onset Caucasian patients.

    Why it matters

    This study looked for mitochondrial DNA variants in 71 late-onset Caucasian patients and found a tRNA(Gln) variant at nucleotide pair 4336 in 5.2% of patients versus 0.7% of controls, plus other variants in individual patients. It reports genetic associations only and does not test any treatment, cure, or prevention.

  20. Atrophy of medial temporal lobes on MRI in "probable" Alzheimer's disease and normal ageing: diagnostic value and neuropsychological correlates.

    ✓ Peer-reviewed alzhub usefulness score 50 out of 100. Journal of Neurology Neurosurgery & Psychiatry 1992-10-01 Brain scans and imaging

    Magnetic resonance imaging (MRI) has shown a great reduction in medial temporal lobe and hippocampal volume of patients with Alzheimer's disease as compared to controls.

    Why it matters

    Visual rating of medial temporal lobe atrophy on plain MRI films distinguished 21 people with Alzheimer's disease from 21 age-matched controls, and the degree of atrophy correlated with mini-mental state examination and memory scores. The authors conclude this atrophy can be assessed quickly and easily and strongly supports a clinical diagnosis of Alzheimer's.

  21. Inverse relationship between education and parietotemporal perfusion deficit in Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 50 out of 100. Annals of neurology 1992-09-01 How common it is

    A higher prevalence of dementia in individuals with fewer years of education has suggested that education may protect against Alzheimer's disease (AD).

    Why it matters

    Patients with probable Alzheimer's who had similar symptom severity but more years of education showed a larger blood-flow deficit in the parietotemporal region (the brain area this pattern links to Alzheimer's), while overall brain blood flow was similar across groups. The authors read this as more advanced disease hidden behind the same symptoms, and propose that education "or its covariates or both" may provide a reserve that delays symptoms. This is a one-time comparison of patient groups using blood flow as a stand-in for pathology. It does not show that education prevents Alzheimer's or that any intervention helps.

  22. Evidence for a membrane defect in Alzheimer disease brain

    ✓ Peer-reviewed alzhub usefulness score 50 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1992-03-01 Down syndrome and Alzheimer's

    To determine whether neurodegeneration in Alzheimer disease brain is associated with degradation of structural cell membrane molecules, we measured tissue levels of the major membrane phospholipids and their metabolites in three cortical areas from postmortem brains of Alzheimer disease patients and matched controls.

    Why it matters

    This study found lower levels of certain structural membrane fats and higher levels of their breakdown products in Alzheimer's brain tissue, suggesting increased breakdown of cell membranes. These findings come from examining brain tissue after death and do not show whether this breakdown causes Alzheimer's or is a result of it.

  23. Prevalence of Alzheimer's disease and other dementias in an elderly urban population: relationship with age, sex, and education

    ✓ Peer-reviewed alzhub usefulness score 50 out of 100. Neurology 1991-12-01 How common it is

    We studied the prevalence of different types of dementia in an elderly population in Stockholm, Sweden, in relation to age, sex, and education.

    Why it matters

    In an elderly Stockholm population, Alzheimer's disease was the most common type of dementia and dementia became more common with age, even in the oldest groups. In contrast to earlier reports, the share of Alzheimer's and vascular dementia was the same across age groups and there were no sex differences by dementia type. Less educated people had more dementia overall, mainly alcoholic and unspecified dementia, but Alzheimer's itself was similarly common at every education level. This prevalence survey shows associations only and does not test treatment or prevention.

  24. Very mild Alzheimer's disease: informant-based clinical, psychometric, and pathologic distinction from normal aging

    ✓ Peer-reviewed alzhub usefulness score 50 out of 100. Neurology 1991-04-01 Getting a diagnosis

    We compare clinicopathologic data from 10 subjects identified in the very mild stage of senile dementia of the Alzheimer type with findings from similar studies in four cognitively normal subjects.

    Why it matters

    In 10 people identified in the very mild stage of Alzheimer-type dementia, memory, language, and speeded psychomotor deficits were found, and plaques and tangles were present in the neocortex in all 10 but essentially absent in four cognitively normal controls. The authors conclude that even questionable dementia can be diagnostic for Alzheimer's disease and that these lesions should suggest clinically undetected disease, but no treatment, cure, or prevention was tested.

  25. Precursor of amyloid protein in Alzheimer disease undergoes fast anterograde axonal transport

    ✓ Peer-reviewed alzhub usefulness score 50 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1990-02-01 Risk genes beyond APOE

    In the brains of aged humans and cases of Alzheimer disease, deposits of amyloid in senile plaques are located in proximity to nerve processes.

    Why it matters

    This study found that amyloid precursor protein undergoes fast anterograde axonal transport in neurons. It describes a basic biological process that may be relevant to how amyloid deposits form, but it does not test any treatment 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.

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