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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Recent increases in human longevity have been accompanied by a rise in the incidence of dementia, highlighting the need to preserve cognitive function in an aging population.
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40/100
The microtubule-associated protein tau oligomerizes, but the actions of oligomeric tau (oTau) are unknown.
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40/100
The basal forebrain cholinergic neurons (BFCN) provide the primary source of cholinergic innervation of the human cerebral cortex.
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40/100
C9orf72 repeat expansions cause inherited amyotrophic lateral sclerosis (ALS)/frontotemporal dementia (FTD) and result in both loss of C9orf72 protein expression and production of potentially toxic RNA and dipeptide repeat proteins.
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During the past decade, accumulating evidence from the research highlights the suggested effects of bacterial communities of the human gut microbiota and their metabolites on health and disease.
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Synaptic and neuronal loss are major neuropathological characteristics of Parkinson's disease.
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The most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) is a GGGGCC repeat expansion in the C9orf72 gene.
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40/100
According to the FDA, aducanumab (Aduhelm), the recently approved anti-Alzheimer drug, reduces the level of cerebral amyloid plaques-a hallmark finding in patients with Alzheimer's disease-and this will result in a reduction in clinical decline.
Why it matters
The authors argue that the apparent reduction in amyloid accumulation seen on PET scans after aducanumab treatment may actually reflect continued and advanced cerebral cell death rather than improvement. They state they are not convinced that amyloid deposits are a hallmark of Alzheimer's disease.
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TREM1 and TREM2 are members of the triggering receptors expressed on myeloid cells (TREM) family.
Why it matters
This review describes the function of TREM1 and TREM2 in liver-related diseases. It is about liver disease and not Alzheimer's disease, so it has no implications for treating, curing or preventing Alzheimer's.
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Vitamin D (Vt. D) is one of the vital hormone having multiple functions in various tissues, including brain.
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Mitochondrial energetic deficit is one of the hallmarks of neurodegenerative disorders, e.g. Alzheimer´s disease (AD).
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In vivo MRI biomarkers can support the diagnosis of early-onset cerebral amyloid angiopathy, which might already be present in pediatric Down syndrome patients.
Why it matters
In 12 children with Down syndrome compared with 12 age-matched controls, this study found significantly more cerebral microbleeds and a higher likelihood of cortical superficial siderosis on MRI. It is a small retrospective imaging study and does not show a treatment or cure.
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Recent research has shown that the triggering receptor expressed on myeloid cells 2 (TREM2) in microglia is closely related to the pathogenesis of Alzheimer's disease (AD).
Why it matters
This article reviews what is known about TREM2 and innate immunity in Alzheimer's disease and states that the mechanism linking them remains unclear. As a review, it reports no new treatment or prevention result.
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Chemotherapy-induced peripheral neuropathy (CIPN) is a common adverse side effect of many antineoplastic agents.
Why it matters
This study is about nerve pain caused by the chemotherapy drug cisplatin in mice, not about Alzheimer's disease. It found that cisplatin-treated mice had persistent pain and sensory deficits, but it does not report any effect on treating, curing or preventing Alzheimer's disease.
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Traumatic brain injury (TBI) is strongly linked to an increased risk of developing dementia, including chronic traumatic encephalopathy and possibly Alzheimer's disease (AD).
Why it matters
In mice expressing human APOE3 or APOE4 isoforms after controlled cortical impact, gene co-expression networks identified Trem2 and Tyrobp as major hubs. This is an animal study of traumatic brain injury, so it does not show whether targeting these genes would treat, cure or prevent Alzheimer's disease.
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Astrocytes and apolipoprotein E (apoE) play critical roles in cognitive function, not only under physiological conditions but also in some pathological situations, particularly in the pathological progression of Alzheimer's disease (AD).
Why it matters
In Alzheimer's disease model mice, deleting apolipoprotein E from astrocytes improved spatial learning and memory, reduced amyloid beta production, and inhibited astrogliosis, apparently through TGF-β/Smad2/STAT3 signaling. These are animal findings and do not establish that targeting astrocyte-derived apolipoprotein E would help people with Alzheimer's disease.
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Mutations in the gene MAPT encoding tau, a microtubules-associated protein, cause a subtype of familial neurodegenerative disorder, known as frontotemporal lobar degeneration tauopathy (FTLD-Tau), which presents with dementia and is characterized by atrophy in the frontal and temporal lobes of the brain.
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Photobiomodulation (PBM) describes the use of red or near-infrared light to stimulate, heal, regenerate, and protect tissue that has either been injured, is degenerating, or else is at risk of dying.
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Frontotemporal dementia (FTD) and other tauopathies characterized by focal brain neurodegeneration and pathological accumulation of proteins are commonly associated with tau mutations.
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40/100
The kynurenine pathway (KP) is the major metabolic pathway of the essential amino acid tryptophan (TRP).
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P021 is a small molecular weight, BBB permeable compound with suitable pharmacokinetics for oral administration, and without adverse effects associated with native CNTF or BDNF molecule.
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Frontotemporal lobar degeneration (FTLD) has been associated with toxic intracellular aggregates of hyperphosphorylated tau (FTLD-tau).
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The incidence of dementia is higher in diabetic patients, but no effective treatment has been developed.
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Bilateral vestibulopathy (BVP) is defined as the impairment or loss of function of either the labyrinths or the eighth nerves.
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40/100
White matter deterioration in the aging human brain contributes to cognitive decline.
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.
- Essential role of the microglial triggering receptor expressed on myeloid cells-2 (TREM2) for central nervous tissue immune homeostasis
- Human immunodeficiency virus type 1 infection alters chemokine beta peptide expression in human monocytes: implications for recruitment of leukocytes into brain and lymph nodes
- Spatial-Temporal Dependency Modeling and Network Hub Detection for Functional MRI Analysis via Convolutional-Recurrent Network
- Astrocytes produce the antiinflammatory and neuroprotective agent hydrogen sulfide
- Effect of Intensive Systolic Blood Pressure Control on Markers of Cerebral Small Vessel Disease by Age
- Extracellular signal-regulated kinase regulates microglial immune responses in Alzheimer's disease
- Beta-amyloid deposition in chronic traumatic encephalopathy
- Astrocytes accumulate A beta 42 and give rise to astrocytic amyloid plaques in Alzheimer disease brains
- Microglial reactivity predicts hippocampal, but not global, atrophy in cerebral small vessel disease
- TREM2 protects from atherosclerosis by limiting necrotic core formation