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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45/100
Huperzine A (HupA), a novel alkaloid isolated from the Chinese herb Huperzia serrata, is a potent, highly specific and reversible inhibitor of acetylcholinesterase(AChE).
Why it matters
Huperzine A, a cholinesterase inhibitor from a Chinese herb, improved cognitive deficits in animal models and protected cells against several toxic insults. These are animal and cell findings, so its usefulness for treating Alzheimer's disease in people is not established here.
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3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) have been reported to reduce the risk of Alzheimer disease.
Why it matters
This laboratory study reports that statins inhibit a beta-amyloid-mediated inflammatory response in microglia through mechanisms independent of cholesterol reduction. It reports no treatment, cure, or prevention tested in patients.
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Alzheimer disease (AD), the most common senile dementia, is characterized by amyloid plaques, vascular amyloid, neurofibrillary tangles, and progressive neurodegeneration.
Why it matters
The study describes how the BRI2 gene binds amyloid-beta precursor protein and inhibits amyloid-beta production, but the mechanisms regulating this processing remain poorly understood. It is a laboratory finding and does not demonstrate a treatment, cure, or prevention for Alzheimer's disease.
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We presently describe the full-length cloning and functional characterization of an HIV-1-inducible gene, astrocyte elevated gene (AEG)-1.
Why it matters
This study cloned and characterized AEG-1, a gene induced in astrocytes by HIV-1, gp120 or TNF-alpha. It is basic laboratory work related to HIV, not a treatment or cure for Alzheimer's disease.
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Together with its adaptor protein, the adaptor protein of 12 kDa also known as KARAP and TYROBP (DAP12), triggering receptor expressed in myeloid cells 2 (TREM2) is a stimulatory membrane receptor of the immunoglobulin/lectin-like superfamily, well known in myeloid cells.
Why it matters
Mutations in TREM2/DAP12 cause a rare inherited disease with bone cysts and "progressive dementia"; when this 2004 study was done, "nothing was known about the role of TREM2/DAP12 in brain cell biology". By staining human and mouse cerebral cortex, the authors found it "strongly expressed by microglia" — the brain's immune cells — and "present in a fraction of neurons but not in astrocytes and oligodendrocytes", with TREM2-carrying neurons "rare" in the hippocampus. It is a tissue-mapping study, not an Alzheimer's study: it gives no numbers and tests no treatment.
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An important aspect of brain cholinesterase function is related to enzymatic differences.
Why it matters
This paper discusses two forms of the enzyme cholinesterase in the brain and suggests that blocking butyrylcholinesterase may raise acetylcholine levels, based on rat brain experiments and clinical data. It does not report a cure or prevention for Alzheimer's disease, and the proposed two-enzyme model remains a hypothesis.
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Familial forms of frontotemporal dementia (FTD) with tauopathy are mostly caused by mutations in the gene encoding the microtubule-associated protein tau (MAPT).
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We recently described the cloning of murine triggering receptor expressed by myeloid cells (TREM) 2, a single Ig domain DNAX adaptor protein 12-associated receptor expressed by cells of the myeloid lineage.
Why it matters
Lab experiments showed that TREM-2, a receptor on myeloid immune cells, binds specifically to a number of bacteria and yeast and to some human astrocytoma cell lines. Binding was blocked by anionic (negatively charged) molecules, suggesting TREM-2 recognizes its targets partly by charge.
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beta-Amyloid(1-42) (A beta 42), a major component of amyloid plaques, accumulates within pyramidal neurons in the brains of individuals with Alzheimer's disease (AD) and Down syndrome.
Why it matters
This study found that astrocytes in Alzheimer's brains accumulate a form of amyloid and may form amyloid plaques after these cells break down. These are observations in human brain tissue and suggest a possible role for astrocytes in plaque formation, but they do not establish a treatment or cure.
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Microglial activation is an early and common feature of almost all neuropathologies, including multiple sclerosis, Alzheimer's disease and mechanical injury.
Why it matters
In adult mice, not all microglia expressed TREM-2, and the share varied between and within brain regions. The authors suggest these regional differences may help explain why brain regions differ in sensitivity to the same harmful signals.
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Enriched populations of human microglial cells were isolated from mixed cell cultures prepared from embryonic human telencephalon tissues.
Why it matters
This laboratory work describes how human microglia were isolated and which immune molecules they produce. It is early cell-level research and does not test any treatment or prevention for Alzheimer's disease.
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Previous demonstrations of hypofrontality in schizophrenia may reflect particular task requirements.
Why it matters
This small imaging study of eight schizophrenia patients found reduced functional connectivity between frontal and temporal brain regions, which was linked to the severity of auditory hallucinations. It concerns schizophrenia, not Alzheimer's disease, and reports no treatment, cure or prevention.
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Severe early stress and maltreatment produces a cascade of events that have the potential to alter brain development.
Why it matters
This review describes how severe early stress and maltreatment can alter stress response systems and brain development, raising the risk of later psychiatric conditions. It concerns childhood stress and trauma and does not test any treatment, cure or prevention for Alzheimer's disease.
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An unusually high frequency of atypical Parkinson syndrome has been delineated over the last 5 years in the French West Indies.
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Proteolytic processing of the transmembrane domain of the amyloid precursor protein (APP) is a key component of Alzheimer's disease pathogenesis.
Why it matters
A new cleavage site in the amyloid precursor protein was identified at Leu-49, beyond the gamma-secretase site, and this cleavage was reduced by presenilin-1 mutants and by gamma-secretase inhibitors. This is basic biochemistry about how APP is cut and does not provide a therapy.
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The viral determinants that underlie human immunodeficiency virus type 1 (HIV-1) neurotropism are unknown, due in part to limited studies on viruses isolated from brain.
Why it matters
This study characterizes HIV-1 isolates from brain and lymphoid tissues and their macrophage tropism and coreceptor use in patients with dementia and HIV-1 encephalitis, which is not Alzheimer's disease. It provides no treatment, cure or prevention for Alzheimer's disease.
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45/100
Hereditary frontotemporal dementia (FTD) is an autosomal dominant neurodegenerative disorder that is associated with mutations in the tau gene and with the pathological accumulation of hyperphosphorylated tau protein in affected brain cells in about a quarter of cases.
Why it matters
In one large family with inherited frontotemporal dementia (not Alzheimer's), the disease was strongly linked to a region of chromosome 17 (lod score 3.46), yet no mutation in the tau gene was found, and brain inclusions stained for ubiquitin but not tau. The authors call this "the first report of ubiquitin-positive, tau-negative inclusions in an FTD family with significant linkage to chromosome 17q21-22"; symptoms began at a mean age of 61.2, most often as loss of initiative and reduced speech. It is a single-family genetic and pathology study and does not test any treatment, cure or prevention.
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Vascular disease causes multi-infarct dementia (MID) or Binswanger's disease (BD), the latter of which is a progressive form of vascular dementia (VaD) associated pathologically with fibrinoid and hyaline changes in brain arterioles with injury to the white matter.
Why it matters
This study examined brain tissue from 5 patients with vascular dementia and found evidence linking matrix metalloproteinases to white matter damage. It is a small postmortem study focused on vascular dementia, not Alzheimer's disease, and does not test any treatment.
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Functional prognosis is poor in an important minority of primary APS patients with > 10 years of disease.
Why it matters
This study followed 39 patients with primary antiphospholipid syndrome for 10 years and found that 15 had organ damage, including 3 with dementia. It is a small observational study of one autoimmune condition, not evidence about treating, curing, or preventing Alzheimer's disease.
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Progressive cerebrovascular atherosclerosis and consecutive stroke are among the most common causes of dementia.
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Huntington's disease (HD) is a fatal inherited neurodegenerative disorder characterized by personality changes, motor impairment, and subcortical dementia.
Why it matters
This study describes transgenic mouse lines for Huntington's disease that show a neurological phenotype and neuronal changes typical of the disease, without evidence of neurodegeneration. It is an animal model of Huntington's disease and does not address treating, curing, or preventing Alzheimer's disease.
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Genetic mutations in the tau gene on chromosome 17 are known to cause frontotemporal dementias.
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Parkinson's disease (PD) is a neurodegenerative disorder that is pathologically characterized by the presence of intracytoplasmic Lewy bodies, the major components of which are filaments consisting of alpha-synuclein.
Why it matters
Alpha-synuclein fibril formation is nucleation-dependent and can be seeded by aggregated alpha-synuclein, with mutant forms able to seed wild-type protein. This is in-vitro Parkinson's disease chemistry with no treatment tested.
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Recently intronic and exonic mutations in the Tau gene have been found to be associated with familial neurodegenerative syndromes characterized not only by a predominantly frontotemporal dementia but also by the presence of neurological signs consistent with the dysfunction of multiple subcortical neuronal circuitries.
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Microglia are a major ghal component of the central nervous system (CNS) and are extremely sessile.
Why it matters
This review describes microglia as sessile central nervous system cells that respond to even minor pathological events, with only perivascular microglia regularly replaced from bone marrow. It reports no treatment, cure or prevention for Alzheimer's disease.
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.
- Neurocytoskeleton Proteins in Cerebrospinal Fluid of People With HIV-1 Subtypes B and C
- Association of olfactory dysfunction with risk for future Parkinson's disease
- Cerebral Amyloid Angiopathy With Progressive Cortical Superficial Siderosis and Convexity Subarachnoid Hemorrhage in an Apolipoprotein E (APOE) ε2/ε2 Homozygous Patient: A Case Report and Literature Review
- TREM2 ectodomain and its soluble form in Alzheimer's disease
- Secreted beta-amyloid precursor protein stimulates mitogen-activated protein kinase and enhances tau phosphorylation
- Cognitive deficits and delayed neuronal loss in a mouse model of multiple microinfarcts
- Histone deacetylase inhibitor valproic acid inhibits cancer cell proliferation via down-regulation of the alzheimer amyloid precursor protein
- A nuclear factor-binding domain in the 5'-untranslated region of the amyloid precursor protein promoter: implications for the regulation of gene expression
- Leukoencephalopathy in normal and pathologic aging: 2. MRI of brain lucencies
- Lipid and Lipoprotein Metabolism in Microglia