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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Intersectins (ITSNs) represent a family of multi-domain adaptor proteins that regulate endocytosis and cell signaling.
Why it matters
This review notes that intersectin proteins have been implicated in Alzheimer disease, but it does not test any treatment or prevention. It is a summary of existing research, not a study showing a way to treat or cure the disease.
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Regular exercise and physical activity provide many health benefits and are encouraged by medical professionals for the primary prevention of and adjuvant treatment of breast cancer Current consensus in the discipline of exercise oncology is that both regular physical activity and exercise training exert some protective effect against breast cancer risk, and may reduce morbidity in some advanced cases.
Why it matters
This review is about exercise, physical activity, and breast cancer, and contains no information on Alzheimer's disease treatment, cure, or prevention. It discusses how exercise might affect tumor-associated macrophages in the tumor microenvironment.
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Individuals with Down syndrome (DS) have high levels of oxidative stress throughout the lifespan.
Why it matters
People with Down syndrome have high oxidative stress throughout life, and this review links that to extra copies of chromosome-21 genes and to mitochondrial damage that is "considered to be a trigger" for Alzheimer's changes in Down syndrome. That link is a working idea, not a proven cause. For families, the key point is that trials of standard antioxidant supplements or diets "have failed to produce uniform therapeutic effect," so this review does not support using them to protect against Alzheimer's.
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It has being shown that glucagon-like peptide-1 (GLP-1), a new anti-diabetes agent, significantly attenuated beta-amyloid (Aβ) levels in rats.
Why it matters
In rats, (Val8)GLP-1 was tested for preventing memory impairment, tau hyperphosphorylation, and ultra-structural changes induced by streptozotocin. This is animal research and does not establish any treatment, cure, or prevention for people.
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To assess the contribution of hyperammonemia and inflammation to induction of mild cognitive impairment (or MHE).
Why it matters
In patients with liver diseases, cognitive impairment appeared before progression to cirrhosis when hyperammonemia and inflammation were high enough, and patients with keloids showed cognitive impairment associated with hyperammonemia and inflammation without liver disease. Hyperammonemia or inflammation alone did not induce cognitive impairment.
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Oxidative stress is known to play a relevant role in Down syndrome (DS) and its effects are documented from embryonic life.
Why it matters
In people with Down syndrome, prolonged coenzyme Q10 treatment produced an age-specific reduction in the percentage of cells with the highest amount of oxidized DNA bases, suggesting a possible role in modulating DNA repair. The earlier shorter trial had shown only a mild protective effect on DNA and was unable to change the overall extent of oxidative damage, so this remains a preliminary finding about oxidative damage rather than a demonstrated treatment for dementia.
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Nasu-Hakola disease (NHD) is a rare autosomal recessive disorder, characterized by a combination of progressive presenile dementia and formation of multifocal bone cysts, caused by genetic mutations of DAP12 and TREM2, which constitute a receptor/adapter signaling complex expressed on osteoclasts, dendritic cells, macrophages, and microglia.
Why it matters
This report describes three siblings in a Japanese family with Nasu-Hakola disease, a rare inherited disorder that includes progressive presenile dementia, caused by a TREM2 splicing mutation. Because it concerns a single family with a rare recessive condition, it does not establish a treatment or prevention for Alzheimer's disease.
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Neurexins (NRXNs) are synaptic cell adhesion molecules having essential roles in the assembly and maturation of synapses into fully functional units.
Why it matters
This laboratory study found that the proteins alpha- and gamma-secretase can sequentially cut neurexin-3β into two fragments, and that this processing is altered by certain presenilin-1 mutations that cause early-onset Alzheimer disease. These are basic cell findings and do not yet indicate a treatment or prevention strategy for people.
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In general, there was only a moderate alteration of gene expression in ADAM10 overexpressing mice.
Why it matters
This study in mice found that overexpressing the alpha-secretase ADAM10 affected many genes and was previously shown to reduce amyloid plaques and cognitive deficits. It is an animal study of gene expression, and it does not show that this approach treats or prevents Alzheimer disease in people.
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Apolipoprotein E (apoE) plays a role in the pathogenesis of Alzheimer disease (AD).
Why it matters
In post-mortem brain tissue, apoE and immunoglobulin G, proteins normally carried in blood, were found inside the walls of small blood vessels damaged by small vessel disease. The worse the vessel damage, the more amyloid beta turned up in nearby support cells (astrocytes); that amyloid was seen in Alzheimer's cases but not in controls. Overall apoE levels did not differ between Alzheimer's and control brains, and the authors call apoE as a link between vessel disease and Alzheimer's a speculation, not a finding. The study did not test any treatment.
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Freezing of gait (FOG), commonly seen in advanced Parkinson's disease (PD), has been classified as its fifth cardinal feature.
Why it matters
This review describes how freezing of gait is common in atypical parkinsonism and in two syndromes, pure akinesia and primary progressive freezing gait, where it is often an early feature. It does not report any treatment, cure, or prevention for Alzheimer's disease.
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Cerebrospinal fluid (CSF) biomarkers have been increasingly studied in dementia clinical and differential diagnosis.
Why it matters
This study compared cerebrospinal fluid tau and beta-amyloid levels in patients with frontotemporal lobar degeneration, Alzheimer disease and controls to see how well they help tell the diseases apart. It is a diagnostic study and does not test any treatment, cure or prevention.
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Down syndrome (DS) provides a model for studying important aspects of Alzheimer disease (AD).
Why it matters
This review describes how chromosome 21 genes including SOD-1 and APP contribute to amyloid beta plaque accumulation, oxidative stress, and neurodegeneration in Down syndrome. It is a mechanistic overview and reports no tested treatment, cure, or prevention.
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The subcellular localization of organelles, mRNAs and proteins is particularly challenging in neurons.
Why it matters
This review discusses whether axonal defects in tau and amyloid precursor protein transgenic animals model axonopathy in Alzheimer's disease. It does not report any treatment, cure, or prevention for Alzheimer's disease.
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Frameshift (+1) proteins such as APP(+1) and UBB(+1) accumulate in sporadic cases of Alzheimer disease (AD) and in older subjects with Down syndrome (DS).
Why it matters
This study found that frameshift proteins accumulate early in young people with Down syndrome and in familial Alzheimer disease, and also in other tauopathies. It suggests these proteins contribute to early dementia, but it does not test any treatment or prevention.
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Collagenous Alzheimer amyloid plaque component (CLAC) is a unique non-Abeta amyloid component of senile plaques (SP) derived from a transmembrane collagen termed CLAC-precursor.
Why it matters
This brain tissue study found that CLAC and Abeta40 or thioflavin S were mostly in separate parts of senile plaques, suggesting CLAC appears early and may slow the maturation of plaques into beta-sheet-rich amyloid. This is laboratory tissue work and does not show a treatment or cure for Alzheimer's disease.
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Immunostaining of adenosine receptors in the hippocampus and cerebral cortex from necropsies of Alzheimer disease (AD) patients shows that there is a change in the pattern of expression and a redistribution of receptors in these brain areas when compared with samples from controls.
Why it matters
This study found adenosine A1 receptors in degenerating neurons with tangles and in the dystrophic neurites of senile plaques in Alzheimer's brain tissue, and A2A receptors appeared in glial cells. It describes where these receptors are located in diseased brain but does not test any treatment, cure or prevention.
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Microglia, residential macrophages in the central nervous system, can release a variety of factors including cytokines, chemokines, etc. to regulate the communication among neuronal and other types of glial cells.
Why it matters
This review notes that hyperactivated microglia may cause neuronal degeneration and that pathological microglial activation has been reported in Alzheimer's disease. It does not report any treatment, cure, or prevention tested in patients.
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The presenilin (PS) proteins are components of the gamma-secretase activity, which is central in the pathogenesis of Alzheimer's disease.
Why it matters
This work describes a new cell-based test for measuring gamma-secretase cleavage of the amyloid precursor protein, with greater sensitivity and specificity. It is a laboratory measurement tool and does not itself treat, cure, or prevent Alzheimer's disease.
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Down syndrome (DS) is the most common chromosomal abnormality associated with early mental retardation and neurological abnormalities followed by precocious age dependent Alzheimer-type neurode generation later in life.
Why it matters
This review discusses protein expression in Down syndrome brain and proposes that abnormalities in coordinated protein expression may be responsible for the neuropathology. It reports no treatment, cure, or prevention for Alzheimer's disease.
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Rasagiline (N-propargyl-1-(R)-aminoindan) is a selective, irreversible monoamine oxidase B (MAO B) inhibitor which has been developed as an anti-Parkinson drug.
Why it matters
In cell and mouse experiments, rasagiline and TV3326 showed neuroprotective and anti-apoptotic activity, and rasagiline reduced effects of traumatic brain injury in mice. This is early laboratory and animal work and does not show a treatment, cure, or prevention for Alzheimer's disease.
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As people with Down syndrome (DS) age, they are at greater risk for Alzheimer disease (AD) than the general population.
Why it matters
In 231 people with Down syndrome, neither presenilin-1 nor alpha-1-antichymotrypsin polymorphisms appeared to increase the risk of dementia, unlike what has been suggested in the general population. A higher frequency of PS-1 heterozygotes was noted in the demented group, but the authors conclude these variants do not have a similar detrimental effect in Down syndrome.
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During a study of the familial aggregation of Down syndrome (DS) and Alzheimer disease (AD), we observed an increase in mosaicism for disomy 21 in older individuals with DS.
Why it matters
This cytogenetic study found that older people with Down syndrome were more likely to have some cells that had lost a copy of chromosome 21, suggesting chromosome loss increases with age. The finding is about cell biology and does not directly address treating, curing, or preventing Alzheimer's disease.
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A 53-year-old Japanese woman with a point mutation in mitochondrial DNA (tRNALeu(UUR), nt3243) consistent with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS) and Alzheimer-type brain pathology is reported.
Why it matters
A single patient with MELAS was found at autopsy to have Alzheimer-type plaques and tangles, and the authors suggest a possible correlation between this mitochondrial DNA abnormality and Alzheimer-type pathology. This is one case report and does not establish a treatment, cure, or prevention.
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Apolipoprotein E (apoE) is a major risk factor for Alzheimer disease (AD), which is the most common cause of progressive dementing illness.
Why it matters
This laboratory study in cultured rat microglia found that these cells can produce apoE mRNA. It is an early cell-culture finding and does not establish any treatment, cure, or prevention for Alzheimer 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.
- Cryptic splicing in synaptic and membrane excitability genes links TDP-43 loss to neuronal dysfunction
- Anti-depression effects of ketogenic diet are mediated via the restoration of microglial activation and neuronal excitability in the lateral habenula
- Prolactin prevents chronic stress-induced decrease of adult hippocampal neurogenesis and promotes neuronal fate
- C9orf72 nucleotide repeat structures initiate molecular cascades of disease
- Neurovascular glial unit: A target of phytotherapy for cognitive impairments
- Late-onset dementia with leukoencephalopathy and a COL4A2 gene variant, causal link or fortuitous association: a case report
- Cerebrospinal fluid sTREM2 levels are associated with gray matter volume increases and reduced diffusivity in early Alzheimer's disease
- Modulation of blood-brain barrier permeability
- Brain iron deposition is linked with cognitive severity in Parkinson's disease
- Higher rates of decline for women and apolipoprotein E epsilon4 carriers