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.
-
Though cerebral white matter injury is a frequently described phenomenon in aging and dementia, the cause of white matter lesions has not been conclusively determined.
Why it matters
In rats, permanently blocking both common carotid arteries to reduce blood flow caused white matter injury and microglial activation after thirteen weeks. This is an animal study, so it cannot yet show whether reduced brain blood flow causes white matter damage in people with dementia.
-
We here report biomagnification (the increasing accumulation of bioactive, often deleterious molecules through higher trophic levels of a food chain) of the neurotoxic nonprotein amino acid beta-methylamino-l-alanine (BMAA) in the Guam ecosystem.
Why it matters
This study reports biomagnification of the neurotoxin BMAA through the Guam food chain, with high concentrations found in flying foxes eaten by the Chamorro people. It notes that Chamorros who died of ALS-PDC, a neurodegenerative disease with symptoms similar to Alzheimer's disease, had BMAA in their brain tissues, which may help explain the high incidence of ALS-PDC among the Chamorro.
-
These findings suggest that long-term treatment with paroxetine is associated with improvement of verbal declarative memory deficits and an increase in hippocampal volume in PTSD.
-
One of the major histopathological hallmarks of Alzheimer's disease (AD) is redundant senile plaques mainly composed of beta-amyloid (Abeta) aggregates.
Why it matters
In cerebrospinal fluid from 81 sporadic Alzheimer's patients and 42 healthy controls, levels of alpha- and beta-secretase cleaved amyloid precursor protein did not differ between groups. However, beta-sAPP was increased in patients with mild cognitive impairment, and alpha-sAPP was lower in Alzheimer's patients carrying the apoE4 allele.
-
Our recently published data on children investigated within 5 days of a PFC showed that children investigated by MRI within 48 h of a PFC had large hippocampal volumes and prolongation of T2 relaxation time.
-
These findings support the hypothesis of reduced serotonin receptor binding in temporal lobe epileptic foci.
-
Amyloid plaques, a major pathological feature of Alzheimer disease (AD), are composed of an internal fragment of amyloid precursor protein (APP): the 4-kd amyloid-beta protein (Abeta).
Why it matters
In brain tissue from 61 people with Alzheimer's disease and 33 people without it, the enzyme BACE (beta-secretase), which carries out one of the two cuts needed to make amyloid-beta, was found at higher levels and with higher activity. The authors report that BACE was raised "in brain regions affected by amyloid deposition" and stayed raised "despite significant neuronal and synaptic loss." This shows that BACE is altered in the Alzheimer's brain. It does not show that BACE causes the disease, and this study did not test any treatment.
-
Accumulation of alpha-synuclein has been associated with neurodegenerative disorders, such as Lewy body disease and multiple system atrophy.
Why it matters
In transgenic mice, expressing human alpha-synuclein from different promoters led to different patterns of alpha-synuclein accumulation, including inclusion bodies in some neurons. This is an animal model study of synuclein pathology, not a treatment or cure.
-
The results confirmed the correlation between hippocampal volumes and neuron cell counts.
-
The microtubule-associated protein tau is a natively unfolded protein in solution, yet it is able to polymerize into the ordered paired helical filaments (PHF) of Alzheimer's disease.
Why it matters
This laboratory study shows that a PHF6* motif in tau promotes aggregation by forming beta-structure, and that the frontotemporal dementia mutations DeltaK280 and P301L aggregate more strongly. It explains how tau clumps form in test systems but tests no treatment or prevention.
-
Nasu-Hakola disease or polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy (PLOSL) is a genetically heterogeneous disease characterized by a combination of systemic bone cysts and dementia.
Why it matters
Nasu-Hakola disease (PLOSL) is a disease that combines bone cysts with dementia; this paper followed eight patients whose diagnosis was confirmed genetically, all carrying two copies of a DAP12 mutation that stops the gene working, and examined autopsy samples from three. In most of them the disease began in their twenties with ankle and wrist pain after strain, followed by fractures from bone cysts; the paper's title describes the dementia as frontal, but the brain findings are not included in this record. It is not a study of Alzheimer's disease and reports no treatment, cure or prevention.
-
Temporoparietal hypoperfusion on SPECT is common to both AD and DLB.
-
The accumulation of alpha-synuclein, ubiquitin and other proteins in Lewy bodies in degenerating dopaminergic neurones in substantia nigra in idiopathic Parkinson's disease (PD) suggest that inhibition of normal/abnormal protein degradation may contribute to neuronal death.
Why it matters
In brain tissue from people with Parkinson's disease, three proteasome activities were reduced in the substantia nigra, and the drug L-dopa did not cause this reduction in vitro. This supports a role for impaired protein breakdown in Parkinson's disease but does not test a treatment.
-
Mutations in the microtubule-associated protein tau, including P301L, are genetically coupled to hereditary frontotemporal dementia with parkinsonism linked to chromosome 17.
Why it matters
Mice expressing human P301L tau developed hyperphosphorylated tau, abnormal filaments, astrocytosis and neuronal apoptosis similar to human tauopathies. It is animal research, so it does not yet show any treatment, cure or prevention for Alzheimer's disease.
-
Recent studies indicate that there is a marked reduction in trkA-containing nucleus basalis neurons in end-stage Alzheimer's disease (AD).
Why it matters
In brain tissue from 30 deceased people, those with mild cognitive impairment and early Alzheimer's disease had fewer nucleus basalis neurons containing trkA. This is a post-mortem finding about early brain changes and does not test any treatment, cure or prevention.
-
The presynaptic protein alpha-synuclein is a prime suspect for contributing to Lewy pathology and clinical aspects of diseases, including Parkinson's disease, dementia with Lewy bodies, and a Lewy body variant of Alzheimer's disease. alpha-Synuclein accumulates in Lewy bodies and Lewy neurites, and two missense mutations (A53T and A30P) in the alpha-synuclein gene are genetically linked to rare familial forms of Parkinson's disease.
Why it matters
Transgenic mice expressing human A53T mutant or wild-type alpha-synuclein developed neuronal alpha-synucleinopathy, neuronal degeneration, and motor defects, with motor neurons particularly vulnerable. This is animal research supporting a role for alpha-synuclein in Lewy body diseases, not a treatment.
-
Pathogenic alpha-synuclein (alphaS) gene mutations occur in rare familial Parkinson's disease (PD) kindreds, and wild-type alphaS is a major component of Lewy bodies (LBs) in sporadic PD, dementia with LBs (DLB), and the LB variant of Alzheimer's disease, but beta-synuclein (betaS) and gamma-synuclein (gammaS) have not yet been implicated in neurological disorders.
Why it matters
In Parkinson's disease and dementia with Lewy bodies, but not normal brains, antibodies to alpha- and beta-synuclein revealed presynaptic axon terminal pathology in the hippocampus, and gamma-synuclein antibodies detected axonal spheroid-like lesions. The findings implicate beta- and gamma-synuclein in these diseases but report no treatment, cure, or prevention.
-
Cerebral amyloid angiopathy (CAA) is associated with apolipoprotein E (APOE gene, apoE protein) polymorphism: current evidence suggests that the epsilon4 allele is a risk factor for the development of CAA and the epsilon2 allele predisposes to hemorrhage.
Why it matters
In cases with cerebral amyloid angiopathy, vascular amyloid, cystatin C, activated microglia, and certain vessel shapes were more frequent in those with hemorrhage, but these features were not associated with the APOE ε2 allele. Only fibrinoid necrosis was associated with the APOE ε2 allele.
-
There is convincing epidemiological and in vitro evidence of chronic oxidative stress in individuals with Down syndrome (DS).
Why it matters
In urine samples from 166 people, this study found significantly elevated markers of oxidative damage to DNA and lipids in those with Down syndrome compared with their siblings. It provides evidence of increased oxidative stress but does not test any treatment, cure or prevention for Alzheimer's disease.
-
In patients with cryptogenic epilepsy, recurrent seizures may cause damage to the hippocampus throughout the lifetime of the patient.
-
The G protein Go is highly expressed in neurons and mediates effects of a group of rhodopsin-like receptors that includes the opioid, alpha2-adrenergic, M2 muscarinic, and somatostatin receptors.
Why it matters
This study created mice lacking the G protein Go, which can be activated by the Alzheimer amyloid precursor protein in vitro, and found the mice had multiple neurological abnormalities and a short half-life of about 7 weeks. It is animal research and does not test any treatment, cure, or prevention of Alzheimer's disease.
-
47/100
Alzheimer's disease (AD) is a devastating neurological disorder characterized by loss of cognitive skills and progressive dementia.
Why it matters
This laboratory study describes how beta-amyloid fibrils activate signaling and superoxide production in microglia, but it states that a direct causal link between beta-amyloid and Alzheimer's disease remains to be established. It offers no treatment, cure or prevention.
-
The difficulty in differentiating progressive supranuclear palsy (PSP, also called Steele-Richardson-Olszewski syndrome) from other related disorders was the incentive for a study to determine the clinical features that best distinguish PSP.
-
In the present study we describe an ELISA to quantify the light subunit of the neurofilament triplet protein (NFL) in CSF.
Why it matters
CSF levels of the neurofilament light protein were higher in patients with ALS and Alzheimer's disease than in controls, and higher in ALS patients with upper motor neuron signs. The authors suggest CSF NFL could be used to monitor neurodegeneration, but this is a measurement study, not a treatment.
-
Human immunodeficiency virus type 1 (HIV-1) infects the brains of a majority of patients with the acquired immunodeficiency syndrome (AIDS), and has been linked to the development of a progressive dementia termed "HIV-associated dementia."
Why it matters
This study localized HIV-1 mainly to macrophages and microglia in the brains of people with AIDS, including some with HIV-associated dementia. It concerns HIV infection in the brain and does not address Alzheimer's disease 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.
- Cutting Edge: Inflammatory Responses Can Be Triggered by TREM-1, a Novel Receptor Expressed on Neutrophils and Monocytes
- Nucleus basalis of Meynert revisited: anatomy, history and differential involvement in Alzheimer's and Parkinson's disease
- Unraveling the conformational landscape of amyloid precursor protein intracellular domain
- The role of tau in neurodegeneration
- Type 2 diabetes mellitus and biomarkers of neurodegeneration
- Implication of dopamine transporter and electroencephalography biomarkers in dementia with lewy bodies
- Synaptic loss in alcohol use disorder: clinical and mechanistic insights from a PET imaging study
- The causal association between resting state intrinsic functional networks and neurodegeneration
- GWAS Identifies 44 Independent Associated Genomic Loci for Self-Reported Adult Hearing Difficulty in UK Biobank
- Mutations in UBQLN2 cause dominant X-linked juvenile and adult-onset ALS and ALS/dementia