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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CVD risk has been associated with white matter lesions known as white matter hyperintensities (WMH) because they produce increased signal on fluid‐attenuated inversion recovery (FLAIR) MRI scans.
Why it matters
This study found no statistically significant link between neighborhood disadvantage and white matter hyperintensities, which are brain changes linked to dementia risk. It does not test any treatment, cure, or prevention.
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In humans, GART [phosphoribosylglycinamide formyltransferase (EC 2.1.2.2) / phosphoribosylglycinamide synthetase (EC 6.3.4.13) / phosphoribosylaminoimidazole synthetase (EC 6.3.3.1)] is a trifunctional protein which catalyzes the second, third, and fifth reactions of the ten step de novo purine synthesis (DNPS) pathway.
Why it matters
This laboratory study compared a HeLa cell line lacking GART with normal HeLa cells and found multiple transcriptome changes, selecting the CD36 gene for initial analysis. The authors discuss pathways and ontologies relevant to Alzheimer's disease and Down syndrome, but this is a cell model of purine synthesis deficiency and does not test any treatment or prevention in people.
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Alzheimer's disease (AD) is a chronic age-related neurodegenerative disease characterized by degeneration of the central cholinergic neurons, inflammation and oxidative stress in the basal forebrain, prefrontal cortex and hippocampus.
Why it matters
In a rat model of Alzheimer-like disease induced by scopolamine, the flavonoid hesperidin was associated with reduced memory impairment and lower levels of TNF-α, IL-1β, Aβ-42, acetylcholinesterase activity, and malondialdehyde, along with higher IL-10 and reduced glutathione. These results in rats suggest hesperidin may have a mitigating role in this Alzheimer-like state, but they are preliminary animal findings and do not establish a treatment for human Alzheimer's disease.
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Astrocytes are specialized glial cells that are essential components of the neurovascular unit (NVU) and are involved in neurodevelopment, brain maintenance and repair, and neurodegeneration.
Why it matters
Extracellular vesicles from Alzheimer disease mouse and patient astrocytes impaired neuroglial and vascular components in laboratory and animal experiments. This suggests a mechanism by which astrocytes may contribute to damage, but it is early laboratory work and no treatment was tested in people.
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Since its first description by Charcot, amyotrophic lateral sclerosis (ALS) has been classified as a single neurodegenerative disease involving motor neurons.
Why it matters
This paper discusses whether ecological factors influence the clinical presentation of amyotrophic lateral sclerosis, a different neurodegenerative disease. It does not report findings on treating, curing, or preventing Alzheimer's disease.
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37/100
Traumatic brain injury (TBI) alters stress responses, which may influence neuroinflammation and behavioral outcome.
Why it matters
In mice given traumatic brain injury, three days of sleep disruption exacerbated and prolonged the inflammatory response. This is an animal study, so it does not establish whether sleep disruption after brain injury affects Alzheimer's disease in humans.
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37/100
The pathogenesis of late-onset Alzheimer's disease (LOAD) mainly involves abnormal accumulation of extracellular β-amyloid (Aβ) and the consequent neurotoxic effects.
Why it matters
In BV-2 cells, TREM2 attenuated Aβ1-42-mediated neuroinflammation by downregulating TLR signaling and promoted Aβ1-42 clearance. This is a cell-based laboratory study, so it does not show whether this mechanism can be used to treat Alzheimer's disease in people.
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Tau protein is located in the axons of neurons and in Alzheimer Disease, is abnormally phosphorylated and aggregates into paired helical filaments (neurofibrillary tangles) reflecting the degree of neurofibrillary pathology and neurodegeneration.
Why it matters
This preliminary study compared serum total tau and phosphorylated tau levels between 42 patients with schizophrenia and 42 healthy controls. It is a small blood-marker comparison and provides no evidence about treating, curing or preventing Alzheimer disease.
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Alzheimer's disease (AD) is pathologically characterized by beta-amyloid (Aβ) plaques and Tau pathology.
Why it matters
In an Alzheimer mouse model, astrocytes were found to make close contact with amyloid plaques but were highly vulnerable to degeneration in cultured brain slices. This is animal and laboratory work and does not test any treatment, cure, or prevention in humans.
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37/100
Down syndrome (DS) is the most common non-lethal genetic condition that affects approximately 1 in 700 births in the United States of America.
Why it matters
This review discusses memory loss and Alzheimer pathology in mouse models of Down syndrome and notes that mechanisms of nerve cell degeneration are largely unexplored. It reports no treatment or cure.
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We previously reported that, in the brains of older patients with vascular dementia (VaD), there is a distinctive accumulation of detergent-extractable soluble amyloid-β, with a predominance of Aβ42 species.
Why it matters
This study measured tau proteins in brain tissue from people with vascular dementia, Alzheimer's disease and normal controls, finding a loss of total tau in vascular dementia. It is about distinguishing these conditions at the tissue level, not about treating or preventing Alzheimer's.
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Microglia are resident mononuclear phagocytes that play a principal role in the maintenance of normal tissue homeostasis in the central nervous system (CNS).
Why it matters
This study profiles PU.1/Spi1 target genes in microglia, noting that microglia accumulate in brain lesions of neurodegenerative diseases such as Alzheimer's disease. It is a gene-profiling study and does not report any treatment, cure, or prevention for Alzheimer's disease.
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Basal forebrain cholinergic neurons play an important role in cognitive functions such as learning and memory, and they are affected in several neurodegenerative diseases, including Alzheimer disease and Down syndrome.
Why it matters
In rat septal cholinergic neurons in culture and in adult brain, the transcription factor Lhx8 regulated TrkA expression and acetylcholine release, and Lhx8 itself was regulated by nerve growth factor in a positive feedback loop. This is an animal and cell study of cholinergic function and does not test any treatment, cure or prevention for Alzheimer's disease.
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Nasu-Hakola disease (NHD) is a rare autosomal recessive disorder, characterized by progressive presenile dementia and formation of multifocal bone cysts, caused by genetic mutations of DNAX-activation protein 12 (DAP12) or triggering receptor expressed on myeloid cells 2 (TREM2).
Why it matters
This immunohistochemical study examined microglia in brains from people with Nasu-Hakola disease, a rare disorder caused by DAP12 or TREM2 mutations. It describes disease pathology in a rare condition and does not establish a treatment, cure or prevention for Alzheimer's disease.
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37/100
Although significant effects of interferon-gamma (IFN-gamma) on glial cells are well documented, information on the expression level and localization of glial IFN-gamma receptors (IFN-gamma-R) in the human central nervous system (CNS) is sparse.
Why it matters
In human central nervous system tissue from Alzheimer disease hippocampus and other neurological cases, almost all interferon-gamma receptor-positive cells corresponded to GFAP-positive astrocytes, while none corresponded to microglia or oligodendrocytes, and a similar pattern was seen in non-neurological cases. In cultured human glial cells the pattern differed, with receptor-positive cells being microglia, astrocytes, or oligodendrocytes depending on the culture, so this basic study reports no treatment, cure, or prevention.
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The finding of postmortem susceptibility-weighted changes in the cerebral cortex of patients with cerebral amyloidosis with a human 7.0-T MR imaging system opens up the possibility of obtaining in vivo radiologic evidence of cerebral amyloid beta deposition.
Why it matters
Using a high-field MRI scanner on postmortem brain tissue, researchers detected changes in all specimens with amyloid deposition and none of the controls. This is a postmortem imaging study and does not test treatment, cure, or prevention.
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Activation of astrocytes has been known to be associated with amyloid-beta (Abeta) deposit and production of pro-inflammatory cytokines and chemokines that lead to neuronal cell death in the pathogenesis of Alzheimer disease (AD).
Why it matters
CCR5 knockout mice showed impaired long-term and spatial memory, increased GFAP, higher Abeta(1-42) levels and elevated BACE1 and C99. These are mouse findings about CCR5 absence and Alzheimer-like changes, not a treatment or prevention result in humans.
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Chronic cerebral hypoperfusion (CCH) increases the risk of Alzheimer disease (AD) through several biologically plausible pathways, but the relationship between CCH and the development of AD remains uncertain.
Why it matters
In rats with chronic cerebral hypoperfusion, BACE1 and amyloid-beta were upregulated and the animals showed cognitive impairment. This links reduced brain blood flow to Alzheimer's-like changes in an animal model but does not test a treatment, cure, or prevention.
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Conditional double knock-out of presenilin-1 (PS1) and presenilin-2 (PS2) (PS cDKO) in forebrain of mice led to progressive memory dysfunction and forebrain degeneration.
Why it matters
In presenilin conditional knock-out mice, this study found increased markers of oxidative stress, notably at 2 months, suggesting oxidative stress is an early event after presenilin loss-of-function. It is an animal study and does not test any treatment, cure or prevention in people.
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We demonstrate that a supernumerary chromosome 21 causes Inhibition of Neuroectodermal DIfferentiation (INDI) of pluripotent ES cells.
Why it matters
In a mouse teratoma model, an extra human chromosome 21 reduced the development of neural tissue and lowered neuron and glia gene markers. This is early animal work related to Down syndrome and does not test any treatment, cure, or prevention for Alzheimer's disease.
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Our results demonstrate that gene expression in trisomy 21 affected placentas significantly differs from that of chromosomally normal placentas, and this difference is only partially explained by over-expression of genes from chromosome 21.
Why it matters
In cultured placental tissue with trisomy 21, about 750 genes were significantly over-expressed, including some implicated in Alzheimer's disease and in ubiquitination and proteosomal degradation. This is a laboratory study of gene expression in placenta and does not test any treatment, cure or prevention for Alzheimer's disease.
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Down syndrome (DS), or trisomy 21, is the most common identifiable genetic cause of mental retardation.
Why it matters
This review describes the cognitive, behavioral and psychiatric profile of people with Down syndrome, noting that behavioral problems occur in about 20% to 40% of children and that internalizing symptoms such as depression and loneliness emerge in adulthood. It notes that early-onset Alzheimer-type dementia and cognitive decline in adulthood can make these symptoms harder to recognize, but it reports no treatment or cure.
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The present study aimed to acquire more information on aging-related alterations, using proteomic and genomic analyses of hippocampus from young (8 months) and old (27 months) rats.
Why it matters
In old versus young rats, hippocampal proteins related to iron-mediated oxidative stress and neurofilament light changed, and the drugs rasagiline and ladostigil reversed aging effects on several genes. This is animal and gene-expression work suggesting oxidative stress and mitochondrial dysfunction as possible targets, not evidence that these drugs treat, cure or prevent Alzheimer's disease in people.
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A disintegrin and metalloprotease (ADAM) transmembrane proteins have metalloprotease, integrin-binding, intracellular signaling and cell adhesion activities.
Why it matters
This review describes ADAM proteins as involved in cleaving amyloid precursor protein and in nervous system development, plasticity and repair. It does not report testing any treatment or prevention for Alzheimer's disease, so it offers no direct evidence that targeting ADAMs would help patients.
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The molecular mechanisms of beta-amyloidogenesis in sporadic Alzheimer's disease are still poorly understood.
Why it matters
In a transgenic mouse model, soluble beta-amyloid rose with age and fibrillary deposits appeared only after 10 months, suggesting oxidative stress and inflammation may relate to amyloid deposition. This is animal-model evidence only and does not show that treating oxidative stress prevents or cures Alzheimer's disease in people.
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.
- Amyloid-β acts as a regulator of neurotransmitter release disrupting the interaction between synaptophysin and VAMP2
- Circulating immune cell phenotypes are associated with inflammatory biomarkers in dementia-free participants from the Framingham Heart Study Offspring cohort
- Mutation in the tau gene in familial multiple system tauopathy with presenile dementia
- Effect of long-term omega 3 polyunsaturated fatty acid supplementation with or without multidomain intervention on cognitive function in elderly adults with memory complaints (MAPT): a randomised, placebo-controlled trial
- Upregulated astrocyte HDAC7 induces Alzheimer-like tau pathologies via deacetylating transcription factor-EB and inhibiting lysosome biogenesis
- Human and mouse single-nucleus transcriptomics reveal TREM2-dependent and TREM2-independent cellular responses in Alzheimer's disease
- The amygdala is enlarged in children but not adolescents with autism; the hippocampus is enlarged at all ages
- An acetylation switch controls TDP-43 function and aggregation propensity
- Noggin Along with a Self-Assembling Peptide Nanofiber Containing Long Motif of Laminin Induces Tyrosine Hydroxylase Gene Expression
- Association of Plasma p-tau181 and p-tau231 Concentrations With Cognitive Decline in Patients With Probable Dementia With Lewy Bodies