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 4,766 studies, highest score first: BibTeX (.bib) · RIS (.ris)
Highest usefulness score first. Studies without a score come last.
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The microtubule-associated tau protein abnormally phosphorylated at threonine 231 (p-tau231) has been investigated as a potential marker of Alzheimer disease.
Why it matters
This study examined whether levels of tau protein phosphorylated at threonine 231 in cerebrospinal fluid relate to the rate at which the hippocampus shrinks in people with Alzheimer disease. It is about using this marker to track structural disease progression, not about treating or preventing the disease.
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Chemokines were originally described as chemotactic cytokines involved in leukocyte trafficking.
Why it matters
This review describes where chemokine receptors are found in the brain, including microglia, astrocytes, oligodendrocytes and neurons, and discusses their possible functions in brain inflammation. It reports no treatment, cure or prevention for Alzheimer's disease.
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The role of microglia recruited from bone marrow (BM) into the CNS during the progression of Alzheimer's disease (AD) is poorly understood.
Why it matters
In mice bred to develop Alzheimer-like amyloid, cells from transplanted bone marrow entered the brain and gathered near amyloid deposits. More of them sat next to amyloid when the transplant was done before amyloid built up than after. In older mice, triggering inflammation in the hippocampus drew in more of these cells and lowered amyloid there. This is mouse research on where brain immune cells come from: it did not test a treatment and reports nothing about memory or about people.
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Tau is the major component of the intracellular filamentous deposits that define a number of neurodegenerative diseases.
Why it matters
This review describes how mutations in the tau gene cause inherited frontotemporal dementia and parkinsonism linked to chromosome 17, and how these mutations affect tau protein or its RNA. It explains disease mechanisms in rare inherited tau disorders and does not report a treatment, cure or prevention for Alzheimer's disease.
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Inflammation is a process that has been actively related with the onset of several neurodegenerative disorders including Alzheimer disease (AD).
Why it matters
This laboratory study describes how the inflammatory cytokine interleukin-6 can lead to Alzheimer-type phosphorylation of tau protein by disrupting the cdk5/p35 pathway. It is early mechanistic work and does not show that blocking this process treats or prevents Alzheimer's disease in people.
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Tg2576 transgenic mice (mice overexpressing the "Swedish" mutation in the human amyloid precursor protein 695) demonstrated a decreased capacity for cell proliferation in the dentate gyrus of the hippocampus compared with non-transgenic littermates at 3 months, 6 months and 9 months of age.
Why it matters
In mice carrying a human APP "Swedish" mutation (Tg2576), being housed alone from weaning further lowered cell proliferation in the hippocampus and "accelerated the age-dependent deposition of beta-amyloid 42 plaques"; the lower proliferation went along with poorer contextual, but not cued, memory. Fluoxetine raised proliferation and improved contextual memory in the isolated mice. This is mouse work and does not show that loneliness causes, or that fluoxetine treats, Alzheimer's disease in people.
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Apoptotic pathways and DNA synthesis are activated in neurons in the brains of individuals with Alzheimer disease (AD).
Why it matters
In cultured primary neurons, familial Alzheimer disease mutants of amyloid precursor protein caused apoptosis and DNA synthesis that were mediated by the kinase PAK3. This is laboratory cell work on a signaling mechanism and does not provide a treatment or cure.
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We have characterized a cluster of single immunoglobulin variable (IgV) domain receptors centromeric of the major histocompatibility complex (MHC) on human chromosome 6.
Why it matters
This describes the human TREM gene cluster on chromosome 6, including TREM1, TREM2 and NKp44, and identifies new related genes. It is basic gene characterization and has no direct implications for treating or preventing Alzheimer's disease.
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46/100
Hyperammonemia resulting from inherited urea cycle enzyme deficiencies or liver failure results in severe central nervous system dysfunction including brain edema, convulsions and coma.
Why it matters
This review concerns hyperammonemia from urea cycle enzyme deficiencies or liver failure, which causes astrocyte changes including Alzheimer Type II astrocytosis. It is about ammonia neurobiology, not Alzheimer's disease, and reports no treatment, cure or prevention for Alzheimer's.
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Neurodegeneration and dementia are common complications of AIDS caused by human immunodeficiency virus type 1 (HIV-1) infection of the central nervous system.
Why it matters
This laboratory study identified human astrocyte genes with increased expression after HIV-1 infection or exposure to HIV-1 envelope glycoprotein. It concerns HIV-related brain effects, not Alzheimer's disease, and does not test any treatment, cure, or prevention for Alzheimer's.
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A collection of 125 PHAL experiments in the rat has been analyzed to characterize the organization of projections from each amygdalar cell group (except the nucleus of the lateral olfactory tract) to the bed nuclei of the stria terminalis, which surround the crossing of the anterior commissure.
Why it matters
This rat anatomy study maps how amygdala cell groups project to the bed nuclei of the stria terminalis. It is basic brain wiring research with no relevance to treating, curing or preventing Alzheimer's disease.
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There is good evidence that the kynurenine pathway (KP) and one of its products, quinolinic acid (QUIN), play a role in the pathogenesis of neurological diseases, in particular AIDS dementia complex.
Why it matters
In cytokine-stimulated cultures of human astrocytes, the cells lacked kynurenine hydroxylase and produced large amounts of kynurenine and kynurenic acid rather than quinolinic acid. This is in-vitro laboratory work with no treatment, cure or prevention demonstrated.
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The age-related neurodegenerative diseases exemplified by Alzheimer&hyp;s disease (AD), Lewy body diseases such as Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), and Huntington&hyp;s disease are characterized by the deposition of abnormal forms of specific proteins in the brain.
Why it matters
This review describes evidence of oxidative damage in the protein deposits of Alzheimer's disease, Parkinson's disease, ALS, and Huntington's disease, and notes that the cause of neuronal death in each appears multifactorial. It is unclear which oxidative damage occurs early versus as a secondary effect, and no treatment is reported.
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Parkinson's disease (PD) is the most common motor disorder affecting the elderly.
Why it matters
In human neuroblastoma cells, iron and free radical generators stimulated formation of alpha-synuclein- and ubiquitin-containing aggregates, and cells overexpressing alpha-synuclein were more vulnerable to iron-induced toxicity. This is a cell study of Parkinson disease mechanisms and does not test any treatment, cure or prevention.
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The numbers of immune-activated brain mononuclear phagocytes (MPs) affect the progression of human immunodeficiency virus (HIV)-1-associated dementia (HAD).
Why it matters
This laboratory and tissue study examined how monocytes migrate through the blood-brain barrier in HIV-associated dementia, a condition different from Alzheimer's disease. It does not provide evidence about treating, curing, or preventing Alzheimer's disease.
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Brain trauma in humans increases the risk for developing Alzheimer disease (AD) and may induce the acute formation of AD-like plaques containing amyloid beta (A beta).
Why it matters
In pigs given diffuse brain injury, amyloid beta and tau accumulated and neurofilament inclusions formed. This is an animal study and does not show that brain trauma causes Alzheimer's disease in people or that any treatment helps.
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AIDS dementia is characterized by neuronal loss in association with synaptic damage.
Why it matters
This laboratory study shows that the HIV-1 protein Tat promotes monocyte transmigration across a model of the human blood-brain barrier and up-regulates CCR5 on human monocytes. It concerns AIDS dementia mechanisms, not Alzheimer's disease treatment or prevention.
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46/100
Chronic overexpression of the neurite growth-promoting factor S100beta has been implicated in the pathogenesis of neuritic plaques in Alzheimer's disease.
Why it matters
This study found that people with Down's syndrome have about twice as many astrocytes overexpressing S100beta as controls across all ages examined. It suggests a possible role for S100beta in plaque formation, but it is an observational study and does not test any treatment or prevention.
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To determine whether cerebrospinal fluid (CSF) viral burden measurements can assist in the evaluation of human immunodeficiency virus (HIV)-associated neurocognitive disorders, we quantified HIV type 1 (HIV-1) RNA in CSF.
Why it matters
Among subjects with AIDS, neuropsychological impairment was associated with significantly higher cerebrospinal fluid HIV-1 RNA levels, while in subjects without AIDS cerebrospinal fluid RNA and neuropsychological impairment were unrelated. It concerns HIV-associated neurocognitive disorders, not the treatment, cure, or prevention of Alzheimer's disease.
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The presence of the APOE epsilon 4 allele encoding apolipoprotein E4 (apoE4) is the major genetic risk factor for late-onset Alzheimer's disease (AD).
Why it matters
This study presents genetic evidence that the apoE receptor LRP may be associated with the expression of late-onset Alzheimer's disease. It is genetic association research and does not provide a treatment, cure, or prevention.
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Hereditary frontotemporal dementia (HFTD) is a rare autosomal dominant form of presenile dementia characterized by behavioral changes and reduced speech.
Why it matters
In three Dutch families with a rare inherited frontotemporal dementia, the gene was traced to chromosome 17q21-q22 (maximum lod score 4.70) and narrowed to a region of about 5 cM; brains showed frontal and temporal shrinkage without Pick bodies. Because three similar disorders had been mapped to the same region, the authors suggest these related dementias "may originate from mutations in the same gene." The study does not identify the gene and does not address diagnosis, treatment or Alzheimer's disease.
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The molecular basis for the degeneration of neurons and the deposition of amyloid in plaques and in the cerebrovasculature in Alzheimer's disease (AD) is incompletely understood.
Why it matters
Transgenic mice expressing the C-terminal 100 amino acids of the amyloid precursor protein developed age-dependent degeneration of neurons and synapses in the hippocampus. These are findings in mice about a possible disease mechanism and do not establish any treatment or prevention for humans.
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Cerebrospinal fluid (CSF) biochemical markers for Alzheimer disease (AD) would be of great value to improve the clinical diagnostic accuracy of the disorder.
Why it matters
In this 1995 study, phosphorylated tau in spinal fluid was higher in people with Alzheimer's disease than in controls, people with Parkinson disease and people with major depression, and 35 of 40 Alzheimer's patients were above the cutoff set from the controls. Levels in vascular and frontal lobe dementia were also raised, with "considerable overlap" with Alzheimer's, so the authors suggested the test may help tell Alzheimer's apart from normal aging, Parkinson disease and depression-related memory problems, but not from those other dementias. They said its sensitivity and specificity still needed to be established, including studies with brain examination after death.
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The apoE epsilon 4 allele may be associated with decreased cognitive function in discordant twin pairs.
Why it matters
In 20 fraternal twin pairs discordant for the apolipoprotein E epsilon 4 allele, twins carrying the allele performed more poorly on cognitive tests than their co-twins without it. This suggests subclinical cognitive changes in normal older adult men with the allele, but no treatment or prevention is tested.
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A spectrum of neurocognitive defects, termed human immunodeficiency virus type 1 (HIV-1)-associated cognitive/motor complex, has been described in patients with acquired immunodeficiency syndrome (AIDS).
Why it matters
This autopsy study describes brain damage and HIV-infected macrophages/microglia in AIDS dementia complex. It concerns HIV-associated dementia, not Alzheimer's disease, and reports no treatment or cure.
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.
- Trafficking and proteolytic processing of APP
- Reduced hippocampal volume in healthy young ApoE4 carriers: an MRI study
- Cell death mechanisms in Parkinson's disease
- TREM2 Inhibits Tau Hyperphosphorylation and Neuronal Apoptosis via the PI3K/Akt/GSK-3β Signaling Pathway In vivo and In vitro
- Mutations in TREM2 lead to pure early-onset dementia without bone cysts
- Divergent patterns of TDP-43 and tau pathologies in primary progressive aphasia
- Intermediate flortaucipir uptake is associated with Aβ-PET and CSF tau in asymptomatic adults
- Trem2 Agonist Reprograms Foamy Macrophages to Promote Atherosclerotic Plaque Stability-Brief Report
- Expression of the phagocytosis-essential protein TREM2 is down-regulated by an aluminum-induced miRNA-34a in a murine microglial cell line
- Cellular forms and functions of brain microglia