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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Intraneuronal accumulation of hyperphosphorylated protein tau in paired helical filaments together with amyloid-beta peptide (Abeta) deposits confirm the clinical diagnosis of Alzheimer disease.
Why it matters
In cultured neurons, membrane depolarization caused a calcium-mediated transient phosphorylation of tau and APP, followed by dephosphorylation. This is a laboratory cell study and does not demonstrate any treatment, cure, or prevention for Alzheimer's disease.
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The proteolytic cleavage of Alzheimer beta-amyloid precursor protein (APP) and signaling receptor Notch is mediated by the PS/gamma-secretase complex, which consists of presenilins, nicastrin, APH-1, and PEN-2.
Why it matters
This laboratory study characterized the APH-1A gene promoter and found that HIF-1 and hypoxia increased gamma-secretase cleavage of APP and Notch. It is molecular cell work and does not show that targeting this pathway treats, cures or prevents Alzheimer's disease.
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The neuropeptide pituitary adenylate cyclase-activating polypeptide (PACAP) has neurotrophic as well as anti-apoptotic properties and is involved in learning and memory processes.
Why it matters
In human neuroblastoma cells, activating the PAC1 receptor with PACAP increased the non-amyloidogenic processing of APP. This was a cell study, so it does not show that PACAP can treat or prevent Alzheimer's disease in people.
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beta-Amyloid peptides (Abeta) that form the senile plaques of Alzheimer disease consist mainly of 40- and 42-amino acid (Abeta 40 and Abeta 42) peptides generated from the cleavage of the amyloid precursor protein (APP).
Why it matters
The small molecule EHT 1864 blocked Rac1 signalling and reduced amyloid-beta 40 and 42 production in vitro and in vivo by modulating APP processing at gamma-secretase. This is early experimental work and does not show a treatment for patients.
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41/100
Transmembrane proteins BRI2 and amyloid precursor protein (APP) co-localize with amyloid beta (Abeta) lesions in sporadic Alzheimer disease and mutations in both precursor proteins are linked to early-onset familial cases of cerebral amyloidosis associated with dementia and/or cerebral hemorrhage.
Why it matters
This study found that the proteins BRI2 and APP interact and that BRI2 regulates amyloid-beta production in cells. It is a laboratory study and does not show any treatment, cure, or prevention for Alzheimer's disease.
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Alzheimer disease is associated with extracellular deposits of amyloid beta-peptides in the brain.
Why it matters
In laboratory cells, blocking glycosphingolipid biosynthesis by inhibiting glycosyl ceramide synthase reduced secretion of amyloid precursor protein and amyloid β peptide. This is cell-based research and does not show a treatment, cure, or prevention for Alzheimer's disease.
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Recent studies have shown that neurofibrillary tangles are frequently accompanied by alpha-synuclein inclusions in sporadic and familial Alzheimer disease, in Down syndrome, in progressive supranuclear palsy, and Parkinsonism dementia complex of Guam.
Why it matters
In two brothers with familial progressive aphasia and frontotemporal dementia, tau pathology was abundant in the hippocampus and basal ganglia, while tau and alpha-synuclein aggregates coexisted only in the nucleus basalis of Meynert. This is a case report about frontotemporal dementia and does not test or propose any treatment, cure or prevention for Alzheimer's disease.
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Polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy (PLOSL) is a recessively inherited disease characterized by early onset dementia associated with bone cysts.
Why it matters
This mouse study shows that the Dap12 and Trem2 genes are expressed together in the brain from embryonic life into adulthood, mainly in microglial cells. It is early laboratory work and does not test any treatment, cure, or prevention for Alzheimer's disease.
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Mitochondria are involved directly in cell survival and death.
Why it matters
This paper discusses rasagiline, an anti-Parkinson drug, and the idea that drugs protecting mitochondrial viability may be cytoprotective. It does not report testing in Alzheimer's disease and does not establish any treatment, cure, or prevention for it.
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Inheritance of the epsilon4 allele for apolipoprotein E (apoE) increases the risk of Alzheimer disease and memory impairment, whereas epsilon2 decreases these risks compared with the most common epsilon3 allele, but the mechanism for these effects is unknown.
Why it matters
In hippocampal slices from mice engineered to carry human APOE2, E3 or E4, long-term potentiation, a laboratory model of memory, was greater in mice with APOE3 than in those with APOE2 or APOE4. This is animal and tissue work that may help investigate how APOE forms affect susceptibility to memory impairment, but it does not yet show anything about treating people.
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The mechanisms underlying blood-brain barrier (BBB) compromise in human immunodeficiency virus (HIV) infection and the ways in which BBB compromise might impair neurocognitive function remain poorly understood.
Why it matters
In 25 people with HIV, more breakdown of the blood-brain barrier on contrast MRI was linked to worse neurocognitive impairment, and patients with high viral load were more impaired. Those on highly active antiretroviral therapy (HAART) had less barrier damage and less impairment for a given level of glial activation. The authors suggest HAART may help protect against HIV-associated dementia partly by preserving the barrier; the study concerns HIV rather than Alzheimer's.
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Niemann-Pick type C1 disease (NPC1) is an autosomal recessive neurovisceral storage disease caused by the mutation of NPC1 gene, resulting in perturbed intracellular transport of unesterified cholesterol.
Why it matters
In brain tissue from 12 patients with Niemann-Pick type C1 disease, abnormal phosphorylated alpha-synuclein was found in most cases and was more intense in those with the APOE ε4 allele. This is a small autopsy study of a different rare disease and does not test treatment for Alzheimer disease.
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41/100
Our data supported the presumption of increased oxidative stress in DS.
Why it matters
People with Down syndrome had higher uric acid levels and higher allantoin levels than controls, and lower levels of hypoxanthine and xanthine, which the authors say supports increased oxidative stress in Down syndrome. This is a blood measurement study and does not test any treatment or prevention.
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The phosphodiesterase inhibitor, ibudilast, has many effects on lymphocytes, endothelial cells, and glial cells.
Why it matters
In neuron and microglia co-cultures, the phosphodiesterase inhibitor ibudilast significantly suppressed neuronal cell death induced by microglial activation with lipopolysaccharide and interferon-gamma. This is cell-culture work and does not establish that ibudilast treats or prevents Alzheimer's disease in people.
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The authors review the clinical, radiological, electrophysiological, pathological, and molecular aspects of Nasu-Hakola disease (polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy or PLOSL).
Why it matters
This review describes Nasu-Hakola disease, a rare condition with bone cysts and dementia leading to death usually in the fifth decade of life. It reports that mutations in DAP12 or TREM2 cause the disease, which informs understanding of these genes but offers no cure.
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Amyloid-beta peptide (Abeta) interacts with the vasculature to influence Abeta levels in the brain and cerebral blood flow, providing a means of amplifying the Abeta-induced cellular stress underlying neuronal dysfunction and dementia.
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There has been an increase of interest in olfactory dysfunction since it was realised that anosmia was a common feature of idiopathic Parkinson's disease (PD) and Alzheimer-type dementia (AD).
Why it matters
This review notes that smell dysfunction is frequent and often severe in Alzheimer disease and may appear before cognitive signs, and that people with anosmia and one APOE-4 allele have an increased risk of later Alzheimer disease. It is a review of smell testing and does not provide a treatment or cure.
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Brain trauma has been shown to be a risk factor for developing Alzheimer disease (AD), and AD-like plaques containing amyloid-beta (Abeta) peptides have been found in the brain shortly following trauma.
Why it matters
In a rat model, brain trauma led to long-term accumulation of amyloid-beta in axons without lasting upregulation of APP genes. This was an animal study, so it does not establish that trauma causes Alzheimer's disease in people or that any intervention prevents it.
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Accumulating evidence supports a role of chemokines and their receptors in brain function.
Why it matters
This study mapped the distribution of the chemokine receptor CXCR4 in adult rat brain and found it in cholinergic and dopaminergic neurons. It is animal anatomy research and does not test any treatment, cure or prevention for Alzheimer's disease.
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Infection with the human immunodeficiency virus (HIV) is associated with a syndrome of cognitive and motor abnormalities that may develop in the absence of opportunistic infections.
Why it matters
This review states that neurons are not productively infected by HIV and that microglia are the predominant resident CNS cell type productively infected by HIV-1, with neurologic dysfunction in HIV-associated dementia appearing to be a consequence of microglial infection and activation. It concerns HIV-associated dementia, not Alzheimer's disease, and does not report a treatment or cure.
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41/100
Cholesterol is implicated to play a role in Alzheimer disease pathology.
Why it matters
This study measured cholesterol-related sterols in the brains of aged amyloid precursor protein transgenic mice. It describes how cholesterol synthesis differs in these mice and does not test any treatment or prevention for Alzheimer's disease.
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Increases in circulating CD14+/CD16+ monocytes have been associated with HIV dementia; trafficking of these cells into the CNS has been proposed to play an important role in the pathogenesis of HIV-induced neurological disorders.
Why it matters
This study of brain specimens found that CD14+/CD16+ monocytes accumulate around blood vessels in HIV encephalopathy and may serve as a reservoir of HIV infection. It concerns HIV dementia and provides no findings about treating, curing or preventing Alzheimer's disease.
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Patients with advanced Parkinson's disease had a significantly higher disease impairment, longer disease duration, and an unstable motor response to levodopa with frequent on-off fluctuations.
Why it matters
This study found that repetitive speech phenomena appeared in 15 of 53 patients with Parkinson's disease, mostly in those with advanced disease and long-term fluctuating symptoms. It is about speech problems in Parkinson's disease, not Alzheimer's disease, and does not provide information on treating, curing or preventing Alzheimer's disease.
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41/100
Several lines of evidence suggest a shared genetic susceptibility to Down syndrome (DS) and Alzheimer disease (AD).
Why it matters
This genetic study found an association between a presenilin-1 gene polymorphism in mothers and a specific type of chromosome error in their children with Down syndrome. It offers a hypothesis about chromosome nondisjunction and does not provide any treatment, cure or prevention for Alzheimer's disease.
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Within the medial temporal lobe, both the hippocampus and amygdala are frequently targeted by researchers and clinicians for volumetric analysis based on magnetic resonance imaging (MRI).
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.
- The process of Lewy body formation, rather than simply α-synuclein fibrillization, is one of the major drivers of neurodegeneration
- Pharmacological inhibition of O-GlcNAcase (OGA) prevents cognitive decline and amyloid plaque formation in bigenic tau/APP mutant mice
- The apolipoprotein E epsilon 4 allele and decline in different cognitive systems during a 6-year period
- Microglia regulation of central nervous system myelin health and regeneration
- Hippocampal myo-inositol and cognitive ability in adults with Down syndrome: an in vivo proton magnetic resonance spectroscopy study
- Microanatomy of the Human Atherosclerotic Plaque by Single-Cell Transcriptomics
- Age and apolipoprotein E*4 allele effects on cerebrospinal fluid beta-amyloid 42 in adults with normal cognition
- The amyloid precursor protein intracellular domain (AICD) as modulator of gene expression, apoptosis, and cytoskeletal dynamics-relevance for Alzheimer's disease
- Central Nervous System Lipoproteins: ApoE and Regulation of Cholesterol Metabolism
- mTOR Hyperactivation in down syndrome hippocampus appears early during development