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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Although age remains the main risk factor to suffer Alzheimer's disease (AD) and vascular dementia (VD), type 2 diabetes (T2D) has turned up as a relevant risk factor for dementia.
Why it matters
In this mouse study, diabetic db/db mice showed cognitive deterioration, brain atrophy, haemorrhages and tau phosphorylation resembling features of both Alzheimer's disease and vascular dementia, while mice with high-fat-diet-induced hyperinsulinemia showed only mild brain changes. The authors suggest controlling glucose homeostasis could improve dementia progress and prognosis, but this is animal research and has not been shown in people.
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Mutations in the TAR DNA Binding Protein gene (TARDBP), encoding the protein TDP-43, were identified in amyotrophic lateral sclerosis (ALS) patients.
Why it matters
This review summarizes TARDBP and FUS mutations found in ALS and notes that TDP-43 inclusions occur in ALS, FTD and other neurodegenerative disorders. It is a genetic summary and does not test any treatment or cure.
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These results suggest that mechanisms leading to atherosclerosis might also lead to an increased number of perivascular spaces.
Why it matters
This study found that perivascular spaces were more frequently found in older participants, in those with hypertension, and in the presence of carotid plaque, suggesting mechanisms leading to atherosclerosis might also lead to more perivascular spaces. The authors state these results need confirmation in prospective studies, and no treatment or prevention is tested.
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Obesity significantly increases the risk of developing type 2 diabetes, hypertension, coronary heart disease, stroke, fatty liver disease, dementia, obstructive sleep apnea and several types of cancer.
Why it matters
This review states that obesity significantly increases the risk of developing dementia, among other diseases. It suggests that a better understanding of adipose tissue dysfunction may provide new therapeutic strategies for treating obesity-induced metabolic diseases.
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Soluble oligomers of the amyloid-β (Aβ) peptide cause neurotoxicity, synaptic dysfunction, and memory impairments that underlie Alzheimer disease (AD).
Why it matters
The study reports that amyloid-beta oligomer binding to the prion protein and downstream Fyn activation depend on cholesterol-rich lipid rafts and the transmembrane LRP1. These are cell and neuron experiments and do not demonstrate a treatment, cure, or prevention for Alzheimer's disease.
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46/100
Therapies designed to decrease the level of SOD1 are currently in a clinical trial for patients with superoxide dismutase (SOD1)-linked familial amyotrophic lateral sclerosis (ALS).
Why it matters
This study examined whether SOD1 protein in cerebrospinal fluid could serve as a marker for antisense oligonucleotide therapy and for ALS, using rats and human samples. It concerns ALS rather than Alzheimer disease and does not test any Alzheimer treatment, cure, or prevention.
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Accumulation of β-amyloid (Aβ) deposits is a primary pathological feature of Alzheimer disease that is correlated with neurotoxicity and cognitive decline.
Why it matters
In 5XFAD mice, nasal treatment with a GSK-3 inhibitor reduced amyloid beta deposits and improved cognitive deficits. This is an animal study and does not establish that GSK-3 inhibition treats Alzheimer's disease in people.
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Biomarkers are needed to improve the sensitivity and accuracy of diagnosis, and also prognosis, in individuals with early Alzheimer disease (AD).
Why it matters
This study found that CSF amyloid and tau protein levels were related to shrinkage of the hippocampus over time in people with very mild Alzheimer's-type dementia. It supports using these markers for prognosis, but it does not test any treatment or prevention.
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Moreover, cognitive correlations with topological network properties suggest their potential use as markers to assess the risk of Alzheimer disease.
Why it matters
The global organization of white matter networks was significantly disrupted in patients with multidomain amnestic mild cognitive impairment, supporting the view that this subtype is a more advanced form of disease than single-domain amnestic mild cognitive impairment. This points to early disruption of whole-brain white matter connectivity in these patients.
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Multiple lines of evidence suggest that specific subtypes of age-related cataract (ARC) and Alzheimer disease (AD) are related etiologically.
Why it matters
This work links a gene region, CTNND2, to both a type of cataract and future Alzheimer-related brain changes, and a rare CTNND2 mutation altered cell behavior and increased secreted amyloid-beta in neuronal cell culture. These are genetic and laboratory findings, not a treatment or prevention result, so they do not yet show any way to treat or prevent Alzheimer's disease.
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Object The authors describe the first clinical trial with encapsulated cell biodelivery (ECB) implants that deliver nerve growth factor (NGF) to the cholinergic basal forebrain with the intention of halting the degeneration of cholinergic neurons and the associated cognitive decline in patients with Alzheimer disease (AD).
Why it matters
This Phase Ib open-label safety study implanted capsules that deliver nerve growth factor to the cholinergic basal forebrain in 6 patients with mild to moderate Alzheimer's disease, and the implants were successfully placed in all patients. It was a small early safety study and does not show that this approach treats, cures or prevents the disease.
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PRD was associated with selective disruption of corticostriatal resting functional MR imaging correlations, which suggests that resting functional MR imaging analyzed in subject-native space may be a useful biomarker in this disease.
Why it matters
This small imaging study compared resting brain connectivity in people with Parkinson-related dementia, Parkinson disease without dementia, and healthy controls. It is about understanding brain changes in Parkinson-related dementia, not about treating, curing or preventing Alzheimer's disease.
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Florbetapir F 18 selectively binds Aβ in human brain tissue.
Why it matters
In brain tissue from 40 people examined after death, how strongly the PET tracer florbetapir F 18 bound matched how much amyloid plaque was found by silver staining, thioflavin S staining and three different Aβ antibodies, and it "did not bind to neurofibrillary tangles." This is tissue-level support for using the tracer to detect amyloid. It does not by itself show how accurate a scan is in a living patient, and it is an imaging agent, not a treatment.
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Down syndrome (DS) is one of the most frequent genetic abnormalities characterized by multiple pathological phenotypes.
Why it matters
This review examines evidence that oxidative stress and impaired mitochondrial function may link Down syndrome to the later development of Alzheimer-like dementia. It proposes molecular pathways for further research and reports no treatment, cure or prevention.
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DCs play a key role in defense against infections and also in preventing inflammatory and autoimmune diseases.
Why it matters
Dendritic cells lacking TREM-2 produced more inflammatory cytokines and type I interferon in response to Toll-like receptor stimulation. The authors suggest TREM-2 sends inhibitory signals after recognizing a ligand made by the cells themselves.
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Tau is a microtubule-associated protein that forms neurofibrillary tangles (NFTs) in the selective vulnerable long projection neurons of the cholinergic basal forebrain (CBF) in Alzheimer's disease (AD).
Why it matters
Examining brain tissue, this study found that tau changes build up in cholinergic basal forebrain neurons as disease progresses from no impairment to mild cognitive impairment to Alzheimer's, and that these changes correlated with cognitive decline. It suggests cognitive changes are linked to early tau events in these neurons before tangles fully form, but it is a tissue study with no treatment tested.
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Neurotrophins, activating the PI3K/Akt signaling pathway, control neuronal survival and plasticity.
Why it matters
This study found that age-dependent accumulation of soluble amyloid-beta oligomers reversed the neuroprotective effect of soluble APP-alpha by modulating the PI3K/Akt-GSK-3beta pathway in a mouse model. It is animal research and does not test any treatment, cure, or prevention in people.
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Alzheimer disease is characterized by accumulation of the β-amyloid peptide (Aβ) generated by β- and γ-secretase processing of the amyloid precursor protein (APP).
Why it matters
This study found that docosahexaenoic acid reduces amyloidogenic processing of APP through multiple mechanisms in vivo and in vitro. It is laboratory and animal research and does not establish that DHA treats, cures, or prevents Alzheimer's disease in people.
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This review of age-related brain microvascular pathologies focuses on topics studied by this laboratory, including anatomy of the blood supply, tortuous vessels, venous collagenosis, capillary remnants, vascular density and microembolic brain injury.
Why it matters
This review of age-related brain microvascular pathology reports that vascular density is decreased in ageing, Alzheimer's disease, and leukoaraiosis, and that cerebrovascular dysfunction precedes and accompanies cognitive dysfunction and neurodegeneration. Hypoperfusion occurs early in Alzheimer's disease, inducing white matter lesions and correlating with dementia, and in vascular dementia cholinergic reductions correlate with cognitive impairment, with cholinesterase inhibitors having some benefit.
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Parkinson's disease is characterized by a progressive loss of dopaminergic neurons in the substantia nigra.
Why it matters
This study reports that CX3CL1 reduces neurotoxicity and microglial activation in a rat model of Parkinson's disease, where neuroinflammation is clearly shown. It is animal work in Parkinson's disease, not a treatment for Alzheimer's disease.
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Rationale the exact etiology of sporadic Alzheimer disease (AD) is unclear, but it is interesting that several cardiovascular risk factors are associated with higher incidence of AD.
Why it matters
In human brain blood-vessel cells grown in the lab, blocking the enzyme that makes nitric oxide raised levels of APP and of BACE1, the enzyme that starts cutting APP into amyloid beta, and increased secreted amyloid beta from 10.93 to 168.21 pg/mL. The authors set out to probe why cardiovascular risk factors, which share reduced nitric oxide in blood vessels, are associated with more Alzheimer's. This is a single cell-culture experiment, not evidence from people and not a treatment or prevention.
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The cholesterol transporter ATP-binding cassette transporter A1 (ABCA1) moves lipids onto apolipoproteins including apolipoprotein E (apoE), which is the major cholesterol carrier in the brain and an established genetic risk factor for late-onset Alzheimer disease (AD).
Why it matters
In amyloid mouse models, the cholesterol transporter ABCA1 was needed for some beneficial effects of the drug GW3965 on apoE levels, and treated mice showed a trend toward reduced amyloid burden. This is animal research and does not show that this approach treats or prevents Alzheimer's disease in people.
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Twenty-one patients showed FDG hypometabolism; the remaining 3 did not.
Why it matters
This study of 24 patients found that patterns of reduced brain glucose metabolism on PET supported classification of progressive apraxia of speech and primary progressive aphasia variants. It concerns imaging patterns in speech and language disorders and does not test any treatment, cure, or prevention for Alzheimer's disease.
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Alzheimer's disease (AD) is the most common progressive dementia and is pathologically characterized by brain deposition of amyloid-beta (Abeta) peptide as senile plaques.
Why it matters
This study in the Tg2576 mouse model of Alzheimer's disease found that overexpression of human S100B exacerbated cerebral amyloidosis and gliosis. Because it was done in mice, it is early and does not establish a treatment, cure, or prevention for people.
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Primary progressive aphasia (PPA) is a clinical dementia syndrome with early symptoms of language dysfunction.
Why it matters
The Northwestern Anagram Test measured sentence production in 16 patients with primary progressive aphasia and correlated with sentence production and aphasia severity. This is a new assessment tool for a language disorder, not a treatment or cure for Alzheimer's 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.
- Cerebral microvascular endothelium and the pathogenesis of neurodegenerative diseases
- Association between presenilin-1 polymorphism and maternal meiosis II errors in Down syndrome
- The intracellular domain of the low density lipoprotein receptor-related protein modulates transactivation mediated by amyloid precursor protein and Fe65
- Astaxanthin Suppresses PM2.5-Induced Neuroinflammation by Regulating Akt Phosphorylation in BV-2 Microglial Cells
- Geniposide ameliorates learning memory deficits, reduces tau phosphorylation and decreases apoptosis via GSK3β pathway in streptozotocin-induced alzheimer rat model
- Selective reduction of astrocyte apoE3 and apoE4 strongly reduces Aβ accumulation and plaque-related pathology in a mouse model of amyloidosis
- Amyloid-beta overproduction causes abnormal mitochondrial dynamics via differential modulation of mitochondrial fission/fusion proteins
- Downregulated miR-29c correlates with increased BACE1 expression in sporadic Alzheimer's disease
- Astroglial plasticity in the hippocampus is affected by chronic psychosocial stress and concomitant fluoxetine treatment
- Lymphatic drainage of the brain and the pathophysiology of neurological disease