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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The convenient synthesis of a focused library (forty molecules) of novel 6,6,5-tricyclic thiazolo[5,4-f]quinazolines was realized mainly under microwave irradiation.
Why it matters
This study describes the synthesis of new compounds that inhibit DYRK1A/1B kinases, which are involved in pathways associated with Alzheimer disease and Down syndrome. The compounds are molecular probes for laboratory research, and the study does not test them in people or show any treatment effect.
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Traumatic brain injury (TBI) is a significant risk factor for chronic traumatic encephalopathy (CTE), Alzheimer's disease (AD), and Parkinson's disease (PD).
Why it matters
In rats after traumatic brain injury, delayed microvascular pathology was linked to prolonged inflammation, blood-brain barrier disruption and progressive white matter damage. This is animal work on brain trauma, so it does not show a treatment or prevention for Alzheimer's disease.
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Cerebrospinal fluid (CSF) tau is a common biomarker for Alzheimer disease (AD).
Why it matters
This study describes a new laboratory method for measuring tau in cerebrospinal fluid using immunoaffinity enrichment and tandem mass spectrometry. It is a technical measurement study and does not test any treatment, cure, or prevention for Alzheimer's disease.
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The estimated incidence of iNPH in a community was higher than those estimated by previous studies where they collected patients at hospitals.
Why it matters
This 10-year follow-up in a rural Japanese community found three new possible cases of idiopathic normal pressure hydrocephalus, with an estimated incidence of 1.2 per 1000 persons per year above age 70. It does not test any treatment, cure or prevention for Alzheimer's disease.
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42/100
Non-neurological surgery has both acute and long-term effects on the brain.
Why it matters
In 35 patients undergoing knee arthroplasty, cerebrospinal fluid total tau increased significantly during and after surgery and correlated with bupivacaine dose, while phosphorylated tau, amyloid-beta 42 and neurofilament light remained unchanged. This concerns effects of non-neurological surgery on biomarkers and does not test a treatment, cure or prevention of Alzheimer disease.
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DJ-1 is an oxidative stress sensor that localizes to the mitochondria when the cell is exposed to oxidative stress.
Why it matters
In cell experiments, reducing DJ-1 in microglia made them more sensitive to dopamine and more likely to release inflammatory cytokines, an effect reduced by rasagiline. This is laboratory work related to Parkinson's disease, not Alzheimer's, and does not establish a treatment for patients.
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Rare non-synonymous variants of TREM2 have recently been shown to be associated with Alzheimer's disease (AD) in Caucasians.
Why it matters
This study tested whether rare TREM2 variants previously linked to Alzheimer's disease in Caucasians showed the same link in 2,190 Japanese people with late-onset Alzheimer's and 2,498 controls. Of the 10 variants checked, only three (R47H, H157Y and L211P) were found, all very rarely (minor allele frequency 0.0002–0.0059), and none showed a significant association with the disease. It is a genetic replication study in one population; it does not show that TREM2 is irrelevant elsewhere and reports no treatment, cure or prevention.
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γ-Secretase generates amyloid β-protein (Aβ), a pathogenic molecule in Alzheimer disease, through the intramembrane cleavage of the β-carboxyl-terminal fragment (βCTF) of β-amyloid precursor protein.
Why it matters
This laboratory study examined how membrane-integrated gamma-secretase associated with lipid rafts cleaves the beta-carboxyl-terminal fragment of amyloid precursor protein. It is basic biochemistry and does not test or establish a treatment, cure or prevention for Alzheimer's disease.
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Alzheimer's disease (AD) involves several possible molecular mechanisms, including impaired brain insulin signaling and glucose metabolism.
Why it matters
In 3xTg-AD mice, injecting streptozotocin into the brain worsened memory impairment, tau hyperphosphorylation and neuroinflammation. This was an animal study, so it does not establish a treatment or prevention for Alzheimer's disease in people.
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In normal adult brain the microtubule associated protein (MAP) tau contains 2-3 phosphates per mol of the protein and at this level of phosphorylation it is a soluble cytosolic protein.
Why it matters
This paper describes how abnormally hyperphosphorylated tau binds normal tau and forms tau oligomers, and that dephosphorylation with protein phosphatase 2A inhibits this while rehyperphosphorylation promotes it. It is a mechanistic account of tau behavior and reports no treatment, cure, or prevention.
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Genetic deficits and loss of function for the triggering receptor expressed in myeloid cells 2 (TREM2; encoded at chr6p21.1), a transmembrane spanning stimulatory receptor of the immunoglobulin/lectin-like gene superfamily, have been associated with deficiencies in phagocytosis and the innate immune system in Alzheimer's disease.
Why it matters
This study found that TREM2 is reduced in Alzheimer's hippocampal tissue and that a microRNA called miRNA-34a targets and lowers TREM2 expression. An experimental anti-miRNA-34a molecule blocked this effect, but this is early laboratory work and does not yet show any treatment benefit in people.
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MicroRNA (miR) dysregulation is found in Alzheimer disease (AD).
Why it matters
The microRNA miR-144 was found to suppress ADAM10 expression and to be up-regulated by activator protein-1, suggesting it may be involved in Alzheimer disease pathogenesis. This is molecular laboratory work and does not show any treatment, cure or prevention.
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The normal on and off switching of the PI3-K (phosphoinositide 3-kinase)/Akt pathway, particularly by its major activators insulin and IGF-1 (insulin-like growth factor-1), is a powerful integrator of physiological responses rudimentary to successful aging.
Why it matters
This review describes how abnormal PI3-K/Akt/mTOR signaling is an early feature in Alzheimer's disease brains and is linked to reduced insulin and IGF-1 responses. It discusses a mechanism and possible drug targets but does not show that any treatment works in patients.
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We report an autopsy case of progressive supranuclear palsy (PSP) that clinically showed only slowly progressive and symmetric upper motor neuron syndrome over a disease course of 12 years.
Why it matters
This single autopsy case showed that when tau pathology was prominent in the motor cortex but minimal in the basal ganglia and brain stem, a person with progressive supranuclear palsy can lack all its classic clinical features and show only a slowly progressive upper motor syndrome. It is one case report and offers no treatment, cure or prevention for Alzheimer's disease.
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Transcriptome study in neurodegenerative disease has advanced considerably in the past 5 years.
Why it matters
This review summarizes gene expression profiling studies in common neurodegenerative diseases and how such studies may reveal disease pathways, therapeutic targets and biomarkers. It reports no new treatment or prevention and is a summary of existing research rather than a clinical trial.
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Our study demonstrated that rTMS improved action naming in subjects with PNFA, possibly due to the modulation of DLPFC pathways and a facilitation effect on lexical retrieval processes.
Why it matters
In 10 patients with progressive non-fluent aphasia, high-frequency repetitive transcranial magnetic stimulation to the left and right dorsolateral prefrontal cortex improved action naming compared with sham stimulation, with no effect on object naming and no effect in patients with semantic dementia. This is a small study of a symptom-focused stimulation and does not test treating, curing or preventing Alzheimer's disease.
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β-Site amyloid precursor protein (APP) cleaving enzyme 1 (BACE1) is the transmembrane aspartyl protease that catalyzes the first cleavage step in the proteolysis of the APP to the amyloid β-protein (Aβ), a process involved in the pathogenesis of Alzheimer disease.
Why it matters
This laboratory work identified a G-rich sequence in BACE1 that forms a G-quadruplex and helps control alternative splicing of the enzyme. It describes a basic mechanism of gene regulation, not a treatment or prevention for Alzheimer's disease.
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Post-translational modification of proteins by the lipid palmitate is critical for protein localization and function.
Why it matters
This review discusses how palmitoylation, controlled by PATs and thioesterases, is important for neuronal and synaptic function and is dysregulated in neuropsychiatric disease. It is a general review and does not show a treatment, cure, or prevention for Alzheimer's disease.
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APP processing and amyloid-β production play a central role in Alzheimer disease pathogenesis.
Why it matters
This laboratory study found that amyloid precursor protein expression is neuron-specific rather than ubiquitous and that its soluble derivatives are highly stable. It describes basic biology of the protein and does not test any treatment, cure, or prevention.
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Dynamic [(11)C]PiB PET can be used successfully to measure cerebral β-amyloid deposition in DS.
Why it matters
This small proof-of-principle study found that PET scanning with Pittsburgh Compound B was safe and acceptable in adults with Down syndrome, and that only those older than 45 showed significant binding in Alzheimer-related brain regions. It is a feasibility study of an imaging method, not a treatment, cure or prevention.
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Activation of astrocytes surrounding amyloid plaques is a hallmark of Alzheimer disease (AD) with consequences yet poorly understood.
Why it matters
This study found altered astroglial connexin immunoreactivity specifically at amyloid plaques in two mouse models of Alzheimer's disease. This is animal work and does not show that targeting connexins would treat or prevent the disease in people.
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A hallmark of Alzheimer disease (AD) is the deposition of amyloid β (Aβ) in brain parenchyma and cerebral blood vessels, accompanied by cognitive decline.
Why it matters
In APP/PS1DeltaE9 mice, deletion of apolipoprotein A-I increased cerebral amyloid angiopathy and worsened memory deficits, while apoA-I reduced amyloid-beta 42 aggregation and toxicity in primary brain cells. This is animal and cell work and does not show a treatment for patients.
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We found differential region-specific associations between degenerative and vascular processes and the structural integrity of the CC across the spectrum of cognitive ability.
Why it matters
In 231 participants, this study found that gray matter volumes and frontal white matter hyperintensities were related to the microstructural integrity of corresponding corpus callosum regions, with vascular risk and cognitive diagnosis showing different patterns. These findings describe how vascular and degenerative processes affect brain connections but do not test any treatment or prevention.
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Abnormal activation of calpain is implicated in synaptic dysfunction and participates in neuronal death in Alzheimer disease (AD) and other neurological disorders.
Why it matters
In a mouse model of Alzheimer's disease, blocking calpain reduced BACE1 expression, amyloid precursor protein processing, and amyloid plaque formation. This suggests that calpain inhibition might slow amyloid plaque development, but the findings come from transgenic mice and have not been tested as a treatment in people.
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The use of miRNAs as biomarkers has gained growing interest in the last few years.
Why it matters
This review discusses microRNAs as potential biomarkers for central nervous system disorders including Alzheimer's disease, noting that they are not yet fully validated. It describes a promising direction for non-invasive diagnosis and early detection, but it does not report a treatment, cure, or prevention.
From across this topic
9 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 9. The same 9 appear here every time.
- TDP-43 nuclear loss in FTD/ALS causes widespread alternative polyadenylation changes
- VAMP-2 is a surrogate cerebrospinal fluid marker of Alzheimer-related cognitive impairment in adults with Down syndrome
- Niche-Specific Reprogramming of Epigenetic Landscapes Drives Myeloid Cell Diversity in Nonalcoholic Steatohepatitis
- Cardiovascular damage, arrhythmogenesis and overlapping Alzheimer and Parkinson's diseases and TDP-43 pathology start in pediatric and young adult urban populations: Magnetic ultrafine particulate matter and industrial particles with motion behavior play a key role
- Associations of modifiable and non-modifiable risk factors with longitudinal white matter hyperintensities, amyloid-β and tau - a prospective cohort study
- Feasibility of Lumbar Puncture in the Study of Cerebrospinal Fluid Biomarkers for Alzheimer's Disease in Subjects with Down Syndrome
- Oxidative stress and the pathogenesis of Parkinson's disease
- Ambient Air Pollution Increases the Risk of Cerebrovascular and Neuropsychiatric Disorders through Induction of Inflammation and Oxidative Stress
- Left lateralized cerebral glucose metabolism declines in amyloid-β positive persons with mild cognitive impairment