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.
-
The purpose of this study was to investigate the potential relationships between cerebrospinal fluid (CSF) measurements of beta-amyloid-1-42 (Abeta(1-42)) and total tau to (11)C-Pittsburgh compound B ((11)C-PiB) and 2-(1-{6-[(2-(18)F-fluoroethyl)(methyl)amino]-2-naphthyl}ethylidene) malononitrile ((18)F-FDDNP) binding as measured using PET.
Why it matters
This study looked at whether cerebrospinal fluid levels of beta-amyloid-1-42 and total tau relate to brain PET binding of two tracers in patients with Alzheimer disease, mild cognitive impairment, and healthy controls. It is a biomarker correlation study and does not test any treatment, cure, or prevention.
-
While sarcasm can be conveyed solely through contextual cues such as counterfactual or echoic statements, face-to-face sarcastic speech may be characterized by specific paralinguistic features that alert the listener to interpret the utterance as ironic or critical, even in the absence of contextual information.
Why it matters
Among people with different neurodegenerative diseases, only the semantic dementia group had trouble understanding sarcasm from vocal and facial cues. Poorer sarcasm comprehension was linked to smaller volume in specific brain regions, which helps explain how these diseases affect social understanding but does not point to a treatment.
-
Triggering receptor expressed in myeloid (TREM) cells 2, a receptor expressed by myeloid cells, osteoclasts and microglia, is known to play a protective role in bones and brain.
Why it matters
This laboratory study identifies Hsp60 as an agonist of the microglial TREM2 receptor, a receptor whose mutations cause a genetic disease affecting bone and brain. It is early mechanistic work and does not test any treatment in patients.
-
Extracellular ATP is a mediator of intercellular communication and a danger signal.
Why it matters
In microglia from mice, amyloid beta triggered calcium increases, ATP release, IL-1beta secretion and membrane permeabilization only when the P2X7 receptor was present. This is laboratory animal and cell research, not a treatment or cure for Alzheimer's disease.
-
The amyloid precursor protein (APP) is cleaved to produce the Alzheimer disease-associated peptide Abeta, but the normal functions of uncleaved APP in the brain are unknown.
Why it matters
This study found that APP is present at excitatory synapses and that NMDA receptor activity regulates APP trafficking and processing, including production of amyloid-beta. It is a laboratory study and does not show any treatment, cure, or prevention for Alzheimer's disease.
-
The beta-amyloid precursor protein (APP) is an orphan transmembrane receptor whose physiological role is largely unknown.
Why it matters
This study found that netrin-1 binds APP and that this binding suppresses amyloid-beta peptide production in brain slices from Alzheimer model transgenic mice. This is a laboratory and animal study and does not show any treatment, cure, or prevention for Alzheimer's disease in humans.
-
Recent findings Corticobasal degeneration and PSP are neurodegenerative diseases characterized by neuronal loss and gliosis in cardinal brain regions, as well as the abnormal deposition of the microtubule associated protein tau in cell bodies and cell processes.
Why it matters
This review highlights that some patients with corticobasal degeneration and progressive supranuclear palsy present with progressive apraxia of speech, nonfluent aphasia, or both. It concerns clinical presentation and diagnosis, not treating, curing, or preventing Alzheimer's disease.
-
Two groups of tau, 3R- and 4R-tau, are generated by alternative splicing of tau exon 10.
Why it matters
This laboratory work shows that extra Dyrk1A, as occurs in Down syndrome, drives alternative splicing of tau toward more 3R-tau, which the authors link to neurofibrillary degeneration. It proposes a mechanism for early tau pathology but tests no treatment, cure or prevention.
-
Amyloid plaques, composed of the amyloid beta-protein (Abeta), are hallmark neuropathological lesions in Alzheimer disease (AD) brain.
Why it matters
This review states that BACE1 initiates amyloid beta generation and that Bace1 knockout mice confirm it as the beta-secretase, making it a suitable drug target. It proposes a treatment strategy but reports no trial or proven therapy.
-
We investigated the changes of sulcal shape (average mean curvature in folded regions and sulcal depth) in mild cognitive impairment (MCI) and Alzheimer's disease (AD) using quantitative surface-based methods in a large sample of magnetic resonance imaging data.
Why it matters
In this MRI study, sulcal widening and shallower sulcal depth were found with disease progression from controls to mild cognitive impairment and from mild cognitive impairment to Alzheimer's disease. The authors say the sulcal widening measurement showed the highest sensitivity in revealing group differences between control and mild cognitive impairment, which might be useful for detecting early dementia.
-
Adults with Down syndrome (DS) develop Alzheimer neurofibrillary degeneration in the brain, but the underlying molecular mechanism is unknown.
Why it matters
This study found that an extra copy of the Dyrk1A gene in Down syndrome leads to overactivity of the Dyrk1A protein, which adds phosphate groups to tau and promotes its clumping, in human brains and a mouse model. These findings suggest a mechanism for nerve cell degeneration but do not provide a treatment or cure.
-
Accumulation of extracellular amyloid beta peptide (Abeta), generated from amyloid precursor protein (APP) processing by beta- and gamma-secretases, is toxic to neurons and is central to the pathogenesis of Alzheimer disease.
Why it matters
This study identified sorting nexin 17 (SNX17) as an adaptor protein that binds amyloid precursor protein and affects its trafficking and processing in early endosomes. It is laboratory cell work on basic biology and reports no treatment, cure or prevention.
-
Beta-amyloid (Abeta) peptides that accumulate in Alzheimer disease are generated from the beta-amyloid precursor protein (betaAPP) by cleavages by beta-secretase BACE1 and by presenilin-dependent gamma-secretase activities.
Why it matters
In cell studies, presenilin deficiency and γ-secretase inhibition lowered BACE1 maturation and activity, and amyloid β42 controlled BACE1 promoter transactivation through NFkappaB. This is laboratory cell research and does not show a treatment, cure, or prevention.
-
Numerous investigations point to the importance of oxidative imbalance in mediating AD pathogenesis.
Why it matters
This study identified 11 proteins with elevated HNE levels in the hippocampus and inferior parietal lobule of people with mild cognitive impairment compared with controls, and enzyme activities of lactate dehydrogenase, ATP synthase and pyruvate kinase were decreased. The authors suggest impairment of target proteins through HNE adducts leads to protein dysfunction and eventually neuronal death, but no treatment was tested.
-
The histological hallmark of Parkinson's disease (PD) is the presence of fibrillar aggregates called Lewy bodies (LBs).
Why it matters
This review describes how Lewy bodies form from alpha-synuclein in Parkinson's disease and notes that recent studies suggest alpha-synuclein oligomers and protofibrils are cytotoxic while Lewy bodies may be protective. It is a summary of existing findings, not a treatment, cure or prevention for Alzheimer's disease.
-
Most individuals with Down syndrome show early onset of Alzheimer disease (AD), resulting from the extra copy of chromosome 21.
Why it matters
This study found that the DYRK1A protein can add phosphate groups to tau at several sites, which reduced tau's ability to support microtubules, in mice and cells. These are laboratory and animal findings that suggest a possible mechanism linking Down syndrome and Alzheimer's disease, but they do not establish a treatment.
-
TDP-43, a nuclear factor that functions in regulating transcription and alternative splicing, was recently identified as a component of the ubiquitin-positive, tau-negative inclusions specific for frontotemporal lobar degeneration (FTLD-U) and amyotrophic lateral sclerosis (ALS).
Why it matters
TDP-43, a protein already known to form tau-negative deposits in frontotemporal lobar degeneration (FTLD-U) and ALS, was also found deposited in the brains of Guamanians with the parkinsonism-dementia complex. The deposits sat in the frontotemporal and hippocampal regions, most were negative for tau, and tissue tests found an abnormal, insoluble 45 kDa form of TDP-43. This is a description of brain tissue from a different disease. It does not study Alzheimer's directly, and it reports no treatment, cure or prevention.
-
46/100
Microglia are the main immune cells of the brain, and under some circumstances they can play an important role in removal of fibrillar Alzheimer amyloid beta peptide (fAbeta).
Why it matters
In cultured mouse cells, brain immune cells called microglia swallowed Alzheimer amyloid fibrils but broke them down poorly. This was not because they lacked digestive enzymes (they had more of many than comparison macrophages) but because their lysosomes were less acidic (average pH about 6), which reduced how well those enzymes worked. Treating the microglia with the inflammatory signals MCSF or interleukin-6 made the lysosomes more acidic and let the cells degrade the amyloid. This is early lab work in mouse cells, not a treatment for people.
-
46/100
Microglia are associated with neuritic plaques in Alzheimer disease (AD) and serve as a primary component of the innate immune response in the brain.
Why it matters
This study examined expression profiles for macrophage alternative activation genes in Alzheimer's disease and mouse models, finding that microglial activation is complex and not fully explored. It does not test or suggest any treatment, cure, or prevention.
-
Biomarkers are needed to assist in the diagnosis and medical management of various neurodegenerative disorders, including Alzheimer's disease (AD), Parkinson's disease (PD), and dementia with Lewy body (DLB).
Why it matters
This preliminary study used a proteomic method to find cerebrospinal fluid proteins that differed in Alzheimer's disease, Parkinson's disease, and dementia with Lewy bodies compared with controls. The authors state the findings must be validated in a larger and different population, and no treatment is tested.
-
The complement system provides an innate defence mechanism against pathogenic microorganisms.
Why it matters
This review describes complement system components in the brain and reports that inflammatory markers are found in Alzheimer's disease brains, suggesting sustained brain inflammation may be a cofactor. It offers no treatment, cure or prevention.
-
Mild to moderate hyperhomocysteinemia is a risk factor for neurodegenerative diseases.
Why it matters
This review describes mechanisms by which homocysteine may damage brain cells, including effects on methylation, calcium influx, amyloid and tau accumulation, and neuronal death, and notes that some effects can be blocked by folate, glutamate receptor antagonists or antioxidants. It is based on laboratory and human observational findings and does not establish a treatment for Alzheimer's disease.
-
A subtle but chronic alteration in metabolic balance between amyloid-beta peptide (Abeta) anabolic and catabolic activities is thought to cause Abeta accumulation, leading to a decade-long pathological cascade of Alzheimer disease.
Why it matters
In mice bred to lack neprilysin and to produce amyloid precursor protein, reduced neprilysin activity led to synapse-associated amyloid-beta oligomers that impaired neuronal plasticity and cognitive function. These are animal findings about how amyloid-beta accumulates and harms synapses, not a proven treatment or prevention for people.
-
Both apolipoprotein E (apoE) and 24(S)-hydroxycholesterol are involved in the pathogenesis of Alzheimer disease (AD).
Why it matters
In this laboratory cell study, 24(S)-hydroxycholesterol increased apoE production and cholesterol efflux in astrocytic cells through a liver X receptor-controlled pathway. This is early, in-vitro work on a mechanism and does not show any treatment, cure or prevention for people.
-
Cases of early-onset Alzheimer disease (AD) with an autosomal dominant inheritance pattern (familial AD [FAD]) are rare but have greatly advanced our understanding of the molecular pathogenesis of AD.
Why it matters
This case report describes a novel presenilin 1 mutation (S170F) causing Alzheimer's disease with Lewy bodies in the third decade of life in one family. It is a genetic and neuropathological description, not a treatment study, so it does not show how to treat, cure or prevent the 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.
- A phase 2 randomized trial of ELND005, scyllo-inositol, in mild to moderate Alzheimer disease
- Microglia modulate neurodegeneration in Alzheimer's and Parkinson's diseases
- Hippocampal volume and neuronal number in Ts65Dn mice: a murine model of Down syndrome
- Mutations of presenilin genes in dilated cardiomyopathy and heart failure
- Systematic Pan-Cancer Analysis Identifies TREM2 as an Immunological and Prognostic Biomarker
- Role of prion protein in mediating the synaptotoxic effects of tau oligomers: Implications for Alzheimer’s disease and related tauopathies
- White matter hyperintensity spatial patterns: Risk factors and clinical correlates
- Abnormal insula functional network is associated with episodic memory decline in amnestic mild cognitive impairment
- Serum phosphate levels are related to all-cause, cardiovascular and COPD mortality in men
- Perfusionsmuster der [18F]PI-2620-Tau-PET bei verschiedenen neurodegenerativen Tauopathien