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.
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Patient A 76-year-old man with a clinical diagnosis of dementia with Lewy bodies underwent fluorodeoxyglucose (18)F and PiB positron emission tomographic brain scans.
Why it matters
In one 76-year-old man diagnosed with dementia with Lewy bodies, a Pittsburgh Compound B (PiB) amyloid scan showed "marked region specific binding", and autopsy 3 months later confirmed the Lewy body diagnosis. The autopsy also found "severe cerebral amyloid angiopathy" (amyloid in blood-vessel walls) but "only moderate numbers" of amyloid plaques. This is a single case: it cannot show how accurate PiB scans are in general, and it tests no treatment.
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Between September 1, 1990, and August 31, 2005, 69 subjects experienced nontraumatic hip or vertebral fractures.
Why it matters
This study found that high-sensitivity C-reactive protein level was a significant and independent risk predictor of nontraumatic fracture in the Bruneck cohort. It does not address dementia, cognition, or Alzheimer's disease, so it provides no information on treating, curing, or preventing Alzheimer's disease.
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Hyperphosphorylated tau protein (P-tau) in CSF is a core biomarker candidate of Alzheimer's disease.
Why it matters
In patients with spinal fluid taken in life and brain examination after death, levels of a phosphorylated tau protein (P-tau231P) in the spinal fluid correlated with the amount of tangle pathology in all neocortical regions studied. The authors say this marker may serve as an in vivo stand-in measure of tangle pathology in Alzheimer's disease.
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Like acetylcholinesterase, butyrylcholinesterase (BChE) inactivates the neurotransmitter acetylcholine (ACh) and is hence a viable therapeutic target in Alzheimer's disease, which is characterized by a cholinergic deficit.
Why it matters
In rats, these BChE inhibitors raised brain acetylcholine, improved cognitive performance, and lowered beta-amyloid peptide. This is animal research only, so it is too early to know whether it would help people with Alzheimer's disease.
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Inflammation has been implicated as a pathogenetic factor in Alzheimer disease, possibly via effects on beta-amyloid (Abeta).
Why it matters
In this small crossover study of 16 healthy adults, induced hyperinsulinemia increased inflammatory markers and Abeta42 in the periphery and the brain. The authors suggest this may potentially increase the risk of Alzheimer's disease, but the study did not test whether it actually causes dementia.
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Accumulating evidence suggests that neurodegeneration induced by pathogenic proteins depends on contributions from surrounding glia.
Why it matters
This laboratory study reports that blocking NF-kappaB signaling in microglia prevented neuronal death caused by amyloid-beta, and that stimulating microglia with amyloid-beta increased acetylation of RelA/p65. It identifies a mechanism in cells, not a treatment, cure or prevention for patients.
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51/100
In Alzheimer disease, increased beta-secretase (BACE1) activity has been associated with neurodegeneration and accumulation of amyloid precursor protein (APP) products.
Why it matters
In APP transgenic mice, lowering BACE1 levels with lentiviral vectors expressing siRNAs reduced amyloid production and neurodegenerative and behavioral deficits. This is an animal study, so it does not establish a treatment, cure, or prevention for Alzheimer's disease in humans.
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The INNO-BIA AlzBio3 selectively and specifically measured Abeta((1-42)), T-TAU, and P-TAU((181P)) in the CSF.
Why it matters
This study developed a new bead-based method that can measure three Alzheimer's-related proteins in cerebrospinal fluid at the same time, and it performed selectively and specifically. The authors conclude this method may be able to replace the older ELISA methods, but the study does not show any treatment, cure, or prevention.
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Multiple system atrophy (MSA) has varying clinical (MSA-P versus MSA-C) and pathological [striatonigral degeneration (SND) versus olivopontocerebellar atrophy (OPCA)] phenotypes.
Why it matters
In a large post-mortem series of people with multiple system atrophy (MSA), a different disease from Alzheimer's, the pattern of brain damage matched the symptoms people had in life: damage centred on the striatonigral system went with the most severe slowness of movement (bradykinesia), and damage centred on the olivopontocerebellar system went with more frequent cerebellar signs. Glial cytoplasmic inclusions became more frequent as neuronal loss became more severe and as disease duration lengthened, but this is a correlation in autopsy tissue. Only 10% of cases also had Lewy body pathology, which the authors read as "not a primary process in MSA". The study tests no treatment and does not apply to Alzheimer's.
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Unesterified cholesterol is an essential structural component of the plasma membrane of every cell.
Why it matters
This review describes cholesterol metabolism in the central nervous system, noting that the brain makes its own cholesterol and that there is no evidence for net transfer of sterol from blood into the brain. It states that whether changes in plasma cholesterol affect cognitive function or the incidence of dementia remains uncertain.
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FSRP and several cardiovascular risk factors were related to both WMHV measured continuously and to a categorical designation of large volumes of WMH.
Why it matters
This study found that a stroke risk profile and several cardiovascular risk factors were related to white matter hyperintensity volume in people without stroke or dementia. It provides evidence of a vascular basis for these brain changes, but does not test any treatment, cure, or prevention.
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The blood-brain barrier (BBB) is a diffusion barrier, which impedes influx of most compounds from blood to brain.
Why it matters
This overview describes the structure and regulation of the blood-brain barrier, including endothelial cells, astrocyte end-feet, pericytes and tight junctions that exclude most blood-borne substances from the brain. It is general background on barrier biology and does not report any treatment, cure or prevention for Alzheimer's disease.
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Insulin has functions in the brain and dysregulation of these functions may contribute to the expression of late-life neurodegenerative disease.
Why it matters
This review summarizes research on insulin's influence on normal brain function and reviews evidence that perturbation of this role may contribute to symptoms and pathogenesis of neurodegenerative disorders including Alzheimer's disease, vascular dementia, Parkinson's disease, and Huntington's disease. The authors conclude by considering whether insulin dysregulation contributes to these disorders through disease-specific or general mechanisms.
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The presence of tangles of abnormally phosphorylated tau is a characteristic of Alzheimer's disease (AD), and the loss of synapses correlates with the degree of dementia.
Why it matters
In a laboratory experiment using microglia and neurons grown together in a dish, microglia activated with secreted beta-amyloid precursor protein or lipopolysaccharide made more IL-1 and TNFα mRNA. When these microglia were placed with neurons, the study reports "a significant increase in the phosphorylation of neuronal tau … accompanied by a decline in synaptophysin levels," and its title attributes these effects to interleukin-1. This is cell-culture work only: it reports no treatment, cure or prevention.
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Human lumbar CSF patterns of Abeta peptides were analysed by urea-based beta-amyloid sodium dodecyl sulphate polyacrylamide gel electrophoresis with western immunoblot (Abeta-SDS-PAGE/immunoblot).
Why it matters
This study found conserved patterns of truncated beta-amyloid peptides in cerebrospinal fluid that distinguished patients with Alzheimer's disease and patients with chronic inflammatory central nervous system disease from other neuropsychiatric diseases. It concerns measurement patterns and provides no treatment, cure or prevention.
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Our objective was to examine whether rapid eye movement (REM) sleep behavior disorder occurs in disproportionally greater frequency in multiple system atrophy (MSA), Parkinson's disease (PD), and dementia with Lewy bodies (DLB), collectively known as the synucleinopathies, compared to other nonsynucleinopathy neurodegenerative disorders.
Why it matters
This study found that REM sleep behavior disorder occurred much more often in people with synucleinopathies such as Parkinson's disease and dementia with Lewy bodies than in those with Alzheimer's disease and other nonsynucleinopathy disorders. It is about distinguishing these conditions, not about treating, curing or preventing Alzheimer's disease.
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We propose the following sequence of events in the development of neuropathologic changes of Alzheimer disease in Down syndrome: (1) intracellular accumulation of Abeta in neurons and astrocytes, (2) deposition of extracellular Abeta and formation of diffuse plaques, and (3) development of neuritic plaques and neurofibrillary tangles with activation of microglial cells.
Why it matters
In 14 autopsy brains from people with Down syndrome aged 11 months to 56 years, the authors saw amyloid beta inside neurons of the youngest brains before it appeared outside cells. From this they proposed a three-step order: amyloid inside cells, then diffuse plaques, then neuritic plaques and tangles. The order was inferred by comparing brains of different ages, not by following anyone over time, and the study offers no treatment or test.
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Triple-A syndrome (MIM 231550; also known as Allgrove syndrome) is an autosomal recessive disorder characterized by adrenocorticotropin hormone (ACTH)-resistant adrenal insufficiency, achalasia of the oesophageal cardia and alacrima.
Why it matters
This study identified a novel gene (AAAS) that is mutant in individuals with triple-A syndrome, a rare autosomal recessive disorder that can include late-onset mild dementia among its neurological symptoms. It is genetic research into a rare syndrome and does not provide a treatment, cure, or prevention for Alzheimer's disease.
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Frontotemporal dementia with parkinsonism, chromosome 17 type (FTDP-17) is caused by mutations in the tau gene, and the signature lesions of FTDP-17 are filamentous tau inclusions.
Why it matters
This laboratory work showed that different tau mutations can increase or decrease inclusion of tau exon 10 by acting on three regulatory elements. It explains one way a tau mutation may cause disease but does not test any treatment, cure or prevention.
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Pallido-ponto-nigral degeneration (PPND) is one of the most well characterized familial neurodegenerative disorders linked to chromosome 17q21-22.
Why it matters
In families with FTDP-17 syndromes including pallido-ponto-nigral degeneration, three tau gene mutations were found, and insoluble tau aggregates from patients' brains contained abnormal tau comigrating with four-repeat isoforms. These genetic and biochemical findings link tau mutations to disease but report no treatment, cure, or prevention.
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51/100
Some cases of autosomal dominant familial amyotrophic lateral sclerosis (FALS) are associated with mutations in the gene encoding Cu/Zn superoxide dismutase (SOD1), suggesting that oxidative damage may play a role in ALS pathogenesis.
Why it matters
Markers of oxidative damage to protein and DNA were increased in the motor cortex of sporadic ALS patients but not in familial ALS patients, and malondialdehyde levels showed no significant changes. This is a tissue study of ALS with no treatment tested.
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Why it matters
Reports that lacking apolipoprotein E dramatically reduces amyloid β-peptide deposition.
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The early endosome is the first vacuolar compartment along the endocytic pathway.
Why it matters
This brain tissue study found that early endosomes in neurons from Alzheimer's brains were enlarged and contained more of certain proteases than in normal brains, suggesting increased endocytic activity. The authors propose this may be a mechanism for increased beta-amyloid formation, but it is descriptive pathology, not a treatment.
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We held an international consensus conference on frontotemporal dementia, behavioral disturbances, and parkinsonism linked to chromosome 17 to determine whether these are homogeneous or heterogeneous disorders, to agree on terminology, and to develop strategies for further research.
Why it matters
An international consensus conference reviewed 13 families with inherited frontotemporal dementia and parkinsonism and agreed that, despite earlier descriptions stressing different features, they "share clinical and neuropathological features," with all linked to the same 2 cM stretch of chromosome 17 (between markers D17S791 and D17S800). It named the condition "frontotemporal dementia and parkinsonism linked to chromosome 17" until the genetic defect was known, and it set finding the responsible gene as the next research step. It identified no gene, tested no treatment, and is not about Alzheimer's disease.
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Onset of falls during the first year are emphasised, as they could lead to an early diagnosis and influence the prognosis of patients with PSP.
Why it matters
In 24 people whose progressive supranuclear palsy (PSP, a condition that is not Alzheimer's disease) was confirmed at autopsy, median survival was 5.6 years (range 2–16.6). Falls in the first year, early swallowing problems and incontinence were linked to shorter survival, while age at onset, sex and early dementia were not. The authors report that diagnostic errors suggest PSP is underdiagnosed, and the study does not address Alzheimer's treatment or prevention.
From across this topic
10 of the 4,748 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.
- Growth hormone secretagogue MK-677: no clinical effect on AD progression in a randomized trial
- The role of tau in the pathological process and clinical expression of Huntington's disease
- Aging-related increase in oxidative stress correlates with developmental pattern of beta-secretase activity and beta-amyloid plaque formation in transgenic Tg2576 mice with Alzheimer-like pathology
- Ultrasensitive RT-QuIC assay with high sensitivity and specificity for Lewy body-associated synucleinopathies
- Diagnosis Across the Spectrum of Progressive Supranuclear Palsy and Corticobasal Syndrome
- Nose to Brain Delivery of Curcumin Loaded Therapeutic Nanostructures for Neurodegenerative Diseases
- Alborixin clears amyloid-β by inducing autophagy through PTEN-mediated inhibition of the AKT pathway
- Common Genetic Variation Indicates Separate Causes for Periventricular and Deep White Matter Hyperintensities
- Bilateral hippocampal volume reduction in adults with post-traumatic stress disorder: a meta-analysis of structural MRI studies
- Axon diodes for the reconstruction of oriented neuronal networks in microfluidic chambers