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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In a variety of neurodegenerative tauopathies including Alzheimer's disease, frontotemporal dementia and some types of Parkinson's disease, tau protein is abnormally hyperphosphorylated by several kinases and eventually aggregates to form neurofibrillary tangles, a neurotoxic pathological characteristic that closely correlates with cognitive impairments.
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The Notch signalling pathway is evolutionarily conserved and is crucial for the development and homeostasis of most tissues.
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36/100
Amyloid-β (Aβ) peptides accumulate in the brain and initiate a cascade of pathologic events in Alzheimer's disease.
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Prion diseases are characterized by accumulation of misfolded protein, gliosis, synaptic dysfunction, and ultimately neuronal loss.
Why it matters
In a mouse model of prion disease, several astrocyte proteins were increased in the brain, but circulating clusterin levels did not differ from controls. This is animal research and does not test a treatment or prevention for Alzheimer's disease in people.
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The hippocampus is essential for the formation and retrieval of memories and is a crucial neural structure sub-serving complex cognition.
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The clinical manifestations that occur after traumatic brain injury (TBI) include a wide range of cognitive, emotional, and behavioral deficits.
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Aggregated Tau proteins are hallmarks of Alzheimer disease and other tauopathies.
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Phenotypic expression of psychopathology may be strongly influenced by exposure to maltreatment, leading to a constellation of ecophenotypes.
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Alzheimer's disease (AD), the most common form of dementia in elderly individuals, is characterized by neurofibrillary tangles, extracellular amyloid-β (Aβ) plaques and neuroinflammation.
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Synaptic loss in the brain correlates well with disease severity in Alzheimer disease (AD).
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The extracellular matrix (ECM) is known to regulate important processes in neuronal cell development, activity and growth.
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Systemic inflammatory events often precipitate acute cognitive dysfunction in elderly and demented populations.
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Late Onset Alzheimer Disease (LOAD) constitutes the majority of AD cases (∼90%).
Why it matters
In aged primates, infantile exposure to lead raised levels of tau and its regulators, suggesting an early-life environmental exposure may contribute to Alzheimer-like tau pathology decades later. This was a study in animals, so it does not show that lead exposure causes Alzheimer's disease in people or that any treatment can prevent it.
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Impairments in mood and cognitive function are the key brain abnormalities observed in Gulf war illness (GWI), a chronic multisymptom health problem afflicting ∼25% of veterans who served in the Persian Gulf War-1.
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Schizophrenia is characterized by reduced hippocampal volume, decreased dendritic spine density, altered neuroplasticity signaling pathways, and cognitive deficits associated with impaired hippocampal function.
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One of the key classical pathological features of Alzheimer's disease (AD) is the progressive accumulation of amyloid beta (Aβ42) peptides and their coalescence into highly insoluble senile plaque cores.
Why it matters
In a mouse microglial cell line, aluminum-induced miRNA-34a reduced TREM2 expression, a protein needed for clearing amyloid beta. This is laboratory cell research only and reports no treatment, cure or prevention for people.
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Increasing evidence suggests that synaptic dysfunction is a key pathophysiological hallmark in neurodegenerative disorders, including Alzheimer's disease.
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Traumatic brain injury (TBI) is a serious problem that affects millions of people in the United States alone.
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Quinolinic acid is a product of tryptophan degradation and may serve as a precursor for NAD(+), an important enzymatic cofactor for enzymes such as the DNA repair protein PARP.
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Diabetic encephalopathy is now accepted as an important complication of diabetes.
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Hippocampal volumes in unmedicated MDD showed evidence of localization to specific subfields and subregions, findings that appear, on the surface, consistent with preclinical evidence for localized mechanisms of hippocampal neuroplasticity.
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Smaller hippocampal volume is reported in major depressive disorder (MDD).
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Proteomics has a wide range of applications, including determination of differences in the proteome in terms of expression and post-translational protein modifications.
Why it matters
This review reports that apolipoprotein A-I levels are decreased and the protein is highly oxidatively modified in serum and cerebrospinal fluid of people with Alzheimer's disease, Parkinson's disease, and Down syndrome with gout. It suggests ApoA-I may be a diagnostic marker and potential therapeutic target, but no treatment is tested.
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Cannabinoids are neuroprotective in models of neurodegenerative dementias.
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Growing evidence suggests that soluble Aβ species can drive Alzheimer disease (AD) pathogenesis by inducing a cascade of events including tau hyperphosphorylation, proteasome impairment, and synaptic dysfunction.
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.
- The role of inflammation in cerebral small vessel disease and vascular cognitive impairment, and therapeutic implications
- X-ray-induced chromatid damage in cells from Down syndrome and Alzheimer disease patients in relation to DNA repair and cancer proneness
- Extracellular Vesicles From 3xTg-AD Mouse and Alzheimer's Disease Patient Astrocytes Impair Neuroglial and Vascular Components
- Growth hormone-releasing hormone effects on brain γ-aminobutyric acid levels in mild cognitive impairment and healthy aging
- Encephalopathy with idiopathic hyperammonaemia and Alzheimer type II astrocytes in equidae
- Neurogranin as a Cerebrospinal Fluid Biomarker for Synaptic Loss in Symptomatic Alzheimer Disease
- Age- and disease-dependent increase of the mitophagy marker phospho-ubiquitin in normal aging and Lewy body disease
- The neuronal transporter gene SLC6A15 confers risk to major depression
- Calcium flux-independent NMDA receptor activity is required for Aβ oligomer-induced synaptic loss
- The neuronal sortilin-related receptor SORL1 is genetically associated with Alzheimer disease