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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42/100
We compared lesions in elderly transgenic (tg) mice carrying the Swedish double mutation KM670/671NL with lesions in Alzheimer disease (AD) by histochemical and immunohistochemical techniques.
Why it matters
In older mice carrying the Swedish APP mutation, amyloid plaques looked "highly similar" to those in human Alzheimer's, with the same ApoE and astrocyte signs — but the mice had no tau tangles, only weak microglia activation and weak complement staining, where human brains showed strong ones. The authors conclude these mice are "only a limited model of AD," so treatments developed in amyloid-overexpressing mice "may be limited in their application" to people. No treatment was tested in this study.
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Neurotoxic side effects of chemotherapy occur frequently and are often a reason to limit the dose of chemotherapy.
Why it matters
This review describes that chemotherapy can cause central neurotoxicity ranging from minor cognitive deficits to encephalopathy with dementia. Management mainly consists of reducing the cumulative dose or lowering dose-intensities, especially in patients at higher risk of neurotoxic side effects.
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42/100
BACE1 is a membrane-bound aspartic protease that cleaves the amyloid precursor protein (APP) at the beta-secretase site, a critical step in the Alzheimer disease pathogenesis.
Why it matters
This laboratory work showed that the Alzheimer's-related enzyme BACE1 can also cleave a sialyltransferase called ST6Gal I. It was done in cells and describes a basic biochemical interaction, not a treatment or prevention for Alzheimer's disease.
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Microglia are endogenous brain macrophages that show distinct phenotypes such as expression of myeloid antigens, ramified morphology, and presence within the neural parenchyma.
Why it matters
This study examines microglia in HIV-1 encephalitis and AIDS dementia, concluding that perivascular macrophages rather than parenchymal microglia are productively infected. It concerns HIV-related brain disease, not Alzheimer's disease treatment or prevention.
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Although DSCR1 (Adapt78) has been associated with successful adaptation to oxidative stress and calcium stress and with devastating diseases such as Alzheimer's and Down syndrome, no rationale for these apparently contradictory findings has been tested.
Why it matters
In cell experiments, this study found that the DSCR1 (Adapt78) protein product calcipressin 1 protected cells against acute oxidative and calcium-mediated stress, while chronic overexpression may be associated with Alzheimer disease progression. It is cell-based work and tests no treatment, cure or prevention in patients.
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Alzheimer disease (AD), the most frequent cause of dementia, is characterized by an important neuronal loss.
Why it matters
In this laboratory study, amyloid-beta 1-42 accumulating inside neurons, but not soluble amyloid-beta outside cells, triggered neuronal apoptosis. This describes a possible mechanism of cell death and does not provide a treatment, cure, or prevention for Alzheimer's disease.
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Tumor necrosis factor (TNF), a proinflammatory cytokine, may be involved in the pathogenesis of Alzheimer disease (AD) based on observations that senile plaques have been found to upregulate proinflammatory cytokines.
Why it matters
A haplotype of three tumor necrosis factor gene variants was associated with late-onset Alzheimer disease in 145 families, supporting a role for inflammation. This is a genetic association study and does not test any treatment.
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Phospholipid composition (mol %) and levels (nmol/mg protein) were determined in postmortem frontal cortical and cerebellar gray matter from older Down Syndrome (DS) patients (age range 38-68 years) and from control subjects.
Why it matters
In postmortem frontal cortex and cerebellum from older people with Down syndrome, total phospholipid content was about 20% lower than in control tissue, with a 37% decrease in phosphatidylinositol and a nearly 35% decrease in ethanolamine plasmalogen. The authors suggest this could reflect loss of dendrites and dendritic spines or a general defect in brain lipid metabolism.
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The precursor of the non-Abeta-component of Alzheimer's disease (AD) amyloid (NACP, alpha-synuclein) aggregates into insoluble filaments of Lewy bodies (LBs) in Parkinson's disease (PD) and dementia with LBs (DLB).
Why it matters
This laboratory study found that tau protein is present in a minority of Lewy bodies in the brains of people with Parkinson's disease and dementia with Lewy bodies. It is a basic tissue study about how proteins aggregate in these conditions, not a test of any treatment, cure, or prevention for Alzheimer's disease.
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Pathological evidence suggests that alterations of the blood-brain barrier (BBB) may occur in association with human immunodeficiency virus (HIV) dementia (HIVD).
Why it matters
This study found elevated cerebrospinal fluid levels of MMP-2, 7 and 9 in association with HIV dementia, suggesting a possible mechanism for blood-brain barrier changes. It concerns HIV dementia, not Alzheimer's disease, and reports no treatment, cure or prevention.
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The cholinergic system is one of the most important modulatory neurotransmitter systems in the brain and controls activities that depend on selective attention, which are an essential component of conscious awareness.
Why it matters
This review discusses the cholinergic system and notes that Alzheimer's disease involves loss of explicit memory and reduced cholinergic activity in the hippocampus and cortex. It describes a disease feature and does not report a tested treatment, cure, or prevention.
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Studies of processing of the Alzheimer beta-amyloid precursor protein (betaAPP) have been performed to date mostly in continuous cell lines and indicate the existence of two principal metabolic pathways: the "beta-secretase" pathway, which generates beta-amyloid (A beta(1-40/42); approximately 4 kDa), and the "alpha-secretase" pathway, which generates a smaller fragment, the "p3" peptide (A beta(17-40/42); approximately 3 kDa).
Why it matters
In primary rat neuronal cultures, this work found that neurons generate both the 4-kDa amyloid-beta peptide and the smaller p3 peptide. It describes basic processing in cells and reports no treatment, cure or prevention for Alzheimer's disease.
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Overexpression of Alzheimer amyloid precursor protein (APP) produces dramatically different phenotypes in transgenic mice depending on the genetic background.
Why it matters
In transgenic mice overexpressing amyloid precursor protein, the phenotype depended on genetic background, SOD1 transgenes were protective, and ablation of Apoe had no significant effect. This is animal research on survival and does not test any treatment, cure, or prevention for Alzheimer's disease.
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A 57-year-old woman showed progressive sensory aphasia as an initial symptom, and then developed total aphasia within 6 years and, finally, severe dementia.
Why it matters
This case report describes a woman with corticobasal degeneration whose cortical lesion focus was in the speech area rather than the frontoparietal region, beginning with progressive aphasia and leading to severe dementia, and a survey of 28 pathologically evaluated cases found two similar cases. It is a case report and review with no treatment, cure or prevention.
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The very low density lipoprotein receptor (VLDL-r) is a cell-surface molecule specialized for the internalization of multiple diverse ligands, including apolipoprotein E (apoE)-containing lipoprotein particles, via clathrin-coated pits.
Why it matters
This study describes where the very low-density lipoprotein receptor is found in the brain, including on microglia near senile plaques, and proposes it may help process apoE and apoE/amyloid complexes. It is descriptive work and does not show any treatment or prevention for Alzheimer disease.
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As in Alzheimer-disease (AD) brain, vacuolated muscle fibers of inclusion-body myositis (IBM) contain abnormally accumulated beta-amyloid precursor protein (beta APP), including its beta-amyloid protein epitope, and increased beta APP-751 mRNA.
Why it matters
This laboratory study found that inserting the beta-amyloid precursor protein gene into cultured normal human muscle fibers caused mitochondrial abnormalities. This is early cell-based work and does not show that the same process happens in Alzheimer's disease or that it can be treated.
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Formalin-fixed postmortem brain tissue from 14 HIV-infected adult patients, with previous repeated neurological and neuroradiological examinations, was studied by immunohistochemical and molecular biological methods.
Why it matters
This postmortem brain study relates expression of HIV Nef and Rev proteins in astrocytes to dementia in HIV-infected patients, which is not Alzheimer's disease. It provides no treatment, cure or prevention for Alzheimer's disease.
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We measured the activities of choline acetyltransferase (ChAT) in the post mortem frontal cortex in 32 Alzheimer's disease (AD) patients with different apolipoprotein E (apoE) genotypes.
Why it matters
In postmortem brain tissue from 32 Alzheimer's patients, those carrying the apolipoprotein epsilon 4 allele had significantly lower levels of the enzyme choline acetyltransferase in the frontal cortex. This indicates a more severe cholinergic deficit in these patients, but the study is observational and does not test any treatment.
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The aetiology and pathogenesis of Alzheimer's disease are currently poorly understood, but symptomatic disease is associated with amyloid plaques, neurofibrillary tangles, neuronal loss and numerous alterations of neurotransmitter systems in the CNS.
Why it matters
In postmortem brains from 11 Alzheimer's cases and five controls, monoamine oxidase B was increased in plaque-associated astrocytes. This describes a brain change and does not test any treatment or prevention.
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Biological effects related to cell growth, as well as a role in the pathogenesis of Alzheimer disease, have been ascribed to the beta-amyloid precursor protein (beta-APP).
Why it matters
The secreted form of beta-amyloid precursor protein stimulated mitogen-activated protein kinases and enhanced tau phosphorylation in cell experiments. This is basic laboratory work on cell signaling and does not show any way to treat, cure or prevent Alzheimer disease.
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The beta-amyloid or beta/A4 peptides that accumulate as filamentous aggregates in the extracellular space of Alzheimer disease (AD) brains are derived from one or more alternatively spliced amyloid precursor proteins (APPs).
Why it matters
This study found that human neurons derived from a teratocarcinoma cell line express only the 695-amino acid APP isoform and produce intracellular amyloid-beta peptides. It is laboratory cell research and does not test any treatment, cure, or prevention.
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The deposition of amyloid in senile plaques and along the walls of the cerebral vasculature is a characteristic feature of Alzheimer disease.
Why it matters
Transgenic mice expressing the carboxyl-terminal fragment of the amyloid precursor protein in the brain showed deposition of beta/A4 immunoreactivity and neuronal pathology. This was an animal study, so it does not establish a treatment, cure or prevention for Alzheimer's disease in people.
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The discovery in the late 1970s that cholinergic neurons in the basal forebrain degenerate in Alzheimer's disease (AD) greatly accelerated research on the role of cholinergic mechanisms in learning and memory.
Why it matters
This review discusses cholinergic mechanisms in learning, memory, and dementia, noting that early enthusiasm for the cholinergic hypothesis has been tempered by subsequent research. Recent findings in humans indicate that antimuscarinic drugs do not model the deficits seen in Alzheimer's disease.
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The tau proteins have been reported only in association with microtubules and with ribosomes in situ, in the normal central nervous system.
Why it matters
This laboratory study in human neuroblastoma cells found tau in the nucleolus and in isolated nuclei, suggesting tau may have functions not directly tied to microtubules. It is early cell-based work and does not show any way to treat or prevent Alzheimer's disease.
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Regional CMRglc (rCMRglc) values were measured with [18F]2-fluoro-2-deoxy-D-glucose (18FDG) and positron emission tomography (PET), using a Scanditronix PC-1024-7B scanner, in 14 healthy, noninstitutionalized subjects with trisomy 21 (Down syndrome; DS) (mean age 30.0 years, range 25-38 years) and in 13 sex-matched, healthy volunteers (mean age 29.5 years, range 22-38 years).
Why it matters
This study found no differences in brain glucose metabolism between young adults with Down syndrome and controls. It shows that metabolism is normal before Alzheimer pathology appears, but it does not test or suggest any 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.
- Flortaucipir F 18 Quantitation Using Parametric Estimation of Reference Signal Intensity
- Time-restricted feeding alters isoflurane-induced memory deficits
- Impairment of cholinergic neurotransmission in adult and aged transgenic Tg2576 mouse brain expressing the Swedish mutation of human beta-amyloid precursor protein
- Analytical Qualification of the BD‐Tau Xplorer kit on LUMIPULSE® G1200
- IGF-1 Provides Protective Role in Arteriosclerotic Cerebral Small Vessel Disease
- Alzheimer's-associated PLCγ2 is a signaling node required for both TREM2 function and the inflammatory response in human microglia
- A TREM2-activating antibody with a blood-brain barrier transport vehicle enhances microglial metabolism in Alzheimer's disease models
- Cholinergic deficiency hypothesis in delirium: a synthesis of current evidence
- The promoter activity of the gene encoding Alzheimer beta-amyloid precursor protein (APP) is regulated by two blocks of upstream sequences
- Phase separation by low complexity domains promotes stress granule assembly and drives pathological fibrillization