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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Ischemic damage to the subcortical white matter of the brain, referred to as leukoaraiosis, is a frequent complication of hypertension-related microvascular disease and contributes to the risk of stroke and vascular dementia.
Why it matters
In these hypertensive siblings, the volume of leukoaraiosis, a type of white matter damage linked to stroke and vascular dementia, showed strong estimated heritability. This suggests genetic factors influence susceptibility to this damage, but it does not test a treatment, cure or prevention for Alzheimer's disease.
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Loss of synapses and dying back of axons are considered early events in brain degeneration during Alzheimer's disease.
Why it matters
Experiments in cells suggest that misregulated tau can block the microtubule tracks used for transport inside axons, which could starve synapses. This is early cell-based work, so it does not yet show that this is what happens in patients or offer a treatment.
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Epidemiological studies of Alzheimer patients from a wide variety of ethnic and socioeconomic backgrounds have identified education and occupation as environmental factors that can affect the risk of developing disease.
Why it matters
This study found that enriched housing, which provides cognitive and social stimulation, worsened amyloid plaque formation in a transgenic mouse model of Alzheimer's disease. It is animal research and does not show that environmental enrichment treats or prevents Alzheimer's disease in people.
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Neurofilaments, a major cytoskeletal constituent of neuronal cells, can be released into the cerebrospinal fluid during several neurodegenerative diseases.
Why it matters
Using a new sensitive ELISA, this study found elevated neurofilament light levels in cerebrospinal fluid across several neurological disorders, including late-onset Alzheimer's disease and vascular dementia. It reports a measurement finding only and does not test any treatment, cure, or prevention for Alzheimer's disease.
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Low density lipoprotein-related protein (LRP) is a transmembrane receptor, localized mainly in hepatocytes, fibroblasts, and neurons.
Why it matters
This laboratory work shows that the low density lipoprotein receptor-related protein is cut by the same gamma-secretase activity that cuts amyloid precursor protein, releasing a fragment that affects signaling involving amyloid precursor protein and Fe65. It describes a basic molecular interaction and does not test any treatment, cure, or prevention of Alzheimer's disease.
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Although the Alzheimer amyloid protein precursor (APP) has been studied intensely for more than a decade, its function in neurons is unresolved.
Why it matters
This study shows that the protein FE65, like amyloid precursor protein (APP), is expressed at high levels in neurons, and that the two together regulate cell movement. It is basic laboratory work on normal protein function and does not test any treatment, cure or prevention for Alzheimer's disease.
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Macrophage/microglia (M phi) are the principal immune cells in the central nervous system (CNS) concomitant with inflammatory brain disease and play a significant role in the host defense against invading microorganisms.
Why it matters
This review describes macrophage/microglia and astrocytes as having a dual role in Alzheimer's disease, multiple sclerosis and HIV-associated dementia, both amplifying inflammation and damage and protecting the CNS. It reports no treatment, cure or prevention.
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Chemokines represent key factors in the outburst of the immune response, by activating and directing the leukocyte traffic, both in lymphopoiesis and in immune surveillance.
Why it matters
This review describes chemokines and their receptors in the central nervous system and their link to AIDS-associated dementia. It does not report a treatment or cure for Alzheimer's disease.
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Differences in regional cerebral blood flow (rCBF) between subjects with Alzheimer's disease (AD), dementia with Lewy bodies (DLB) and healthy volunteers were investigated using statistical parametric mapping (SPM99).
Why it matters
This study compared regional cerebral blood flow patterns in 48 patients with Alzheimer's disease, 23 with dementia with Lewy bodies, and 20 healthy controls using SPET scans. It describes imaging differences between dementias and does not test any treatment, cure, or prevention.
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Inheritance of apoE4 is a strong risk factor for the development of late-onset sporadic Alzheimer's disease (AD).
Why it matters
In laboratory experiments, melatonin blocked the formation of amyloid fibrils promoted by apolipoprotein E4 and prevented toxicity to neuronal cells in culture. These findings are preliminary and suggest that age-related reductions in brain melatonin might contribute to a proamyloidogenic environment, but no human treatment is established.
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We previously showed the non-steroidal anti-inflammatory drug (NSAID) ibuprofen suppresses inflammation and amyloid in the APPsw (Tg2576) Tg2576 transgenic mouse.
Why it matters
This study found that six months of ibuprofen treatment in transgenic mice reduced open field behavior and showed reduced caspase activation per plaque, but the effects were not mediated by changes in APP expression or oxidative damage. It is animal research and does not show that ibuprofen treats or prevents Alzheimer's disease in people.
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Mounting evidence suggests that cholesterol may contribute to the pathogenesis of Alzheimer disease (AD).
Why it matters
Using two staining techniques, this study found abnormal cholesterol accumulation in the dense cores of senile plaques in Alzheimer's brains and in transgenic APP(SW) mice. It describes where cholesterol is found in diseased tissue and reports no treatment, cure or prevention.
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Latency to onset of dysarthria and dysphagia clearly differentiated PD from the APDs, but did not help distinguish different APDs.
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We have previously shown that Alzheimer disease (AD) brain exhibits terminal deoxynucleotidyl transferase dUTP nick end-labeling (TUNEL) for DNA damage and morphological evidence for apoptosis.
Why it matters
Brain tissue from people with Down syndrome and Alzheimer's disease showed increased TUNEL labeling for DNA damage and some apoptotic morphologies compared with controls. This is a post-mortem tissue study of cell death mechanisms and does not test any treatment.
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Tau polymerization into the filaments that compose neurofibrillary tangles is seminal to the development of many neurodegenerative diseases.
Why it matters
This laboratory study describes a laser light scattering method to measure how tau protein forms filaments, and used it to study mutant tau from a rare inherited dementia. It is in-vitro work and does not test any treatment, cure or prevention in people.
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Many neurodegenerative diseases are associated with the abnormal sequestration of disease-specific proteins in the brain, but the events that initiate this process remain unclear.
Why it matters
In beta-amyloid precursor protein-transgenic mice, infusing brain extracts from Alzheimer's patients induced A beta deposition after five months. This is an animal study showing that A beta deposition can be seeded, but it does not establish a treatment, cure, or prevention for Alzheimer's disease in people.
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The epsilon 4 allele of apolipoprotein E (APOE) has been found to be a risk factor for late-onset Alzheimer's disease (AD).
Why it matters
In laboratory experiments, zinc- and copper-induced clumping of beta-amyloid was highest when apolipoprotein E4 was present, matching the higher Alzheimer risk linked to the epsilon 4 allele. This is in-vitro work only and does not show that preventing this clumping treats or prevents Alzheimer disease in people.
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Microglia are the main human immunodeficiency virus (HIV) reservoir in the central nervous system and most likely play a major role in the development of HIV dementia (HIVD).
Why it matters
This laboratory study shows that microglia express CCR5, CXCR4 and CCR3, with CCR5 as the principal coreceptor for HIV-1 dementia isolates. It concerns HIV dementia, not Alzheimer's disease, and provides no treatment, cure or prevention for Alzheimer's disease.
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The presenilin (PS) genes associated with Alzheimer disease encode polytopic transmembrane proteins which undergo physiologic endoproteolytic cleavage to generate stable NH2- and COOH-terminal fragments (NTF or CTF) which co-localize in intracellular membranes, but are tightly regulated in their stoichiometry and abundance.
Why it matters
In cultured cells and brain, presenilin 1 fragments were found together in a roughly 250-kDa complex that also contains beta-catenin but not amyloid precursor protein. This describes basic protein biology and does not test any treatment or prevention.
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Oxidative stress has been proposed as a pathogenetic mechanism in Parkinson's disease (PD).
Why it matters
Nitrotyrosine, a marker of oxidative protein damage, was found in Lewy bodies and deposits in the brains of people with Parkinson's disease. The authors state this does not yet provide a definitive link between oxidative stress and neuronal dysfunction, and no treatment is reported.
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The precursor of the non-Abeta component of Alzheimer's disease amyloid (NACP) (also known as a-synuclein) is a presynaptic terminal molecule that accumulates in the plaques of Alzheimer's disease.
Why it matters
In brain tissue from several disorders, alpha-synuclein labeled Lewy bodies, abnormal neurites and plaque dystrophic neurites, but not neurofibrillary tangles, Pick bodies or other tau-positive structures. This is a tissue-staining study and does not test any treatment, cure or prevention.
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Apolipoprotein E (apoE) is associated with several classes of plasma lipoproteins and mediates uptake of lipoproteins through its ability to interact with specific cell surface receptors.
Why it matters
This study found apoE and apoA-I genes in zebrafish, a non-mammalian vertebrate, and showed they are highly expressed during embryonic development. It is early animal research and does not test any treatment, prevention, or cure for Alzheimer's disease in people.
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Animal models are an important aid in experimental medical science because they enable one to study the pathogenetic mechanisms and the therapeutic principles of treating the functional disturbances (symptoms) of human diseases.
Why it matters
This review compares animal models of Parkinson's disease with the human disease and discusses how neurotoxic agents can imitate its features. It does not test any treatment or prevention for Alzheimer's disease, so it has no direct implications for treating, curing, or preventing the disease.
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The beta-amyloid precursor protein (beta-APP), from which the beta-A4 peptide is derived, is considered to be central to the pathogenesis of Alzheimer disease (AD).
Why it matters
Transgenic mice expressing the 751-amino acid isoform of human beta-amyloid precursor protein showed age-dependent deficits in spatial learning and spontaneous alternation. This is animal work linking APP to learning problems and does not provide a treatment for people.
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Germ-line and somatic mtDNA mutations are hypothesized to act together to shape our history and our health.
Why it matters
This paper discusses how inherited and somatic mitochondrial DNA mutations may predispose people to late-onset degenerative diseases, noting a tRNA(Gln) mutation at nucleotide pair 4336 in some Alzheimer and Parkinson disease cases. It is a broad discussion of mitochondrial genetics and does not report a treatment, cure, 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.
- Participation of presenilin 2 in apoptosis: enhanced basal activity conferred by an Alzheimer mutation
- Repetitive speech phenomena in Parkinson's disease
- Metallothionein-I-II and GFAP positivity in the brains from frontotemporal dementia patients
- Quantitative Polymerase Chain Reaction Does not Improve Preoperative Prostate Cancer Staging: A Clinicopathological Molecular Analysis of 121 Patients
- What causes the hippocampal volume decrease in depression? Are neurogenesis, glial changes and apoptosis implicated?
- Phase Separation of FUS Is Suppressed by Its Nuclear Import Receptor and Arginine Methylation
- Abeta is targeted to the vasculature in a mouse model of hereditary cerebral hemorrhage with amyloidosis
- A mouse model for Down syndrome exhibits learning and behaviour deficits
- Gene expression and functional deficits underlie TREM2-knockout microglia responses in human models of Alzheimer's disease
- Gonadal function in young women with Down syndrome