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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Nerve Growth Factor (NGF) supports neuronal survival, plasticity, and growth by binding to p75NTR and TrkA receptors.
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Alzheimer’s Disease (AD) is characterised by the progressive depletion of Acetylcholine (ACh), a neurotransmitter essential for cognition and synaptic communication.
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Postmitotic neurons must preserve genome integrity for decades despite continuous oxidative, transcription-associated, and environmental DNA damage.
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16/100
Neurodegenerative proteinopathies are defined by distinct proteins whose folding, trafficking and clearance depend on shared proteostasis machinery.
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Scrapie, a prion disease, is usually considered a protein-only infection.
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Amyloid β-protein (Aβ), which is known for its role in Alzheimer's disease (AD), is also involved in several physiological functions.
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Although dementias primarily affect memory, they also disrupt our closest social relationships, resulting in elevated caregiver burden and worse patient outcomes.
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Early neuronal hyperexcitability is a hallmark of Alzheimer’s disease (AD) and correlates with cognitive decline.
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We built a computer model that reproduces the rhythms and, crucially, lets the measured timing between slow waves and spindles control how strongly memories are written into cortex.
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Approved Alzheimer’s disease therapies fail to address the two drivers of cognitive decline: loss of BDNF-TrkB signalling and accumulation of hyperphosphorylated tau protein.
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A key pathophysiological hallmark of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) is loss of nuclear localization and abnormal cytoplasmic aggregation of TAR DNA-binding protein 43 (TDP-43).
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Endosomal dysfunction is a presymptomatic hallmark of neurodegeneration.
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Intracellular neurofibrillary tangles formed from hyperphosphorylated tau and extracellular amyloid plaques containing aggregated Aβ-peptides, specific cleavage products of the Amyloid Precursor Protein (APP), are the primary histopathological hallmarks of Alzheimer’s Disease (AD), the leading cause of dementia in humans.
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Amyloid β (Aβ) plaques are a hallmark of Alzheimer’s disease (AD).
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2µM FAM labelled β-amyloid 1–40 was transported through CLEFF4 cells with an apparent permeability (Papp) of 4.47x10 − 6 cm/sec in the efflux direction (Basolateral (Bas) to apical (Ap)) while Ap to Bas direction was only 1.67x10 − 6 cm/sec.
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Neurodegenerative diseases posit a global challenge due to their aging-dependent increasing incidence around the world.
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Drugs that target APP have already been developed for AD and our data suggests they offer an exciting opportunity for repurposing in the treatment of prostate cancer.
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Alzheimer’s Disease (AD) is characterised by two histopathological hallmarks, intracellular tau-containing neurofibrillary tangles and extracellular amyloid plaques containing β-amyloid (Aβ), a specific cleavage product of Amyloid Precursor Protein (APP).
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Alzheimer's disease (AD) is characterized by the deposition of amyloid-beta (Aβ) and microtubule-associated protein tau (MAPT) neurofibrillary tangles in the brain; however, the molecular mechanisms underlying associated synaptic dysfunction remain unclear.
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Neurotrophins regulate neuronal survival, differentiation, and synaptic plasticity through activation of tropomyosin receptor kinase (Trk) receptors, and their dysregulation is strongly implicated in neurodegenerative disorders, including Alzheimer’s disease.
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Pathogenic tau oligomers are transmitted between neurons and non-neuronal cells and may contribute to cellular dysfunction in Alzheimer’s disease (AD).
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Structural studies of amyloid fibrils extracted from brain tissue have identified disease-specific fibril polymorphs.
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16/100
Circadian disruption, notably sleep disturbances, serves as an early indicator of Alzheimer’s disease (AD), preceding cognitive symptoms like memory loss.
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The Klotho (KL) gene encodes a single-pass transmembrane protein that functions as a potent suppressor of aging.
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Alzheimer's disease (AD) is a multifactorial neurodegenerative disorder for which effective multitarget therapies remain unavailable.
From across this topic
10 of the 1,352 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.
- Neurotoxic Soluble Amyloid Oligomers Drive Alzheimer's Pathogenesis and Represent a Clinically Validated Target for Slowing Disease Progression
- Systems-based proteomics to resolve the biology of Alzheimer's disease beyond amyloid and tau
- Accumulation of dipeptide repeat proteins predates that of TDP ‐43 in frontotemporal lobar degeneration associated with hexanucleotide repeat expansions in C9ORF72 gene
- Neurofibrillary tangles of Alzheimer's disease brains contain 14-3-3 proteins
- Familial Alzheimer's disease patient-derived neurons reveal distinct mutation-specific effects on amyloid beta
- α-Enolase reduces cerebrovascular Aβ deposits by protecting Aβ amyloid formation
- Anti-acetylated-tau immunotherapy is neuroprotective in tauopathy and brain injury
- Preclinical and Clinical Development of ABBV-8E12, a Humanized Anti-Tau Antibody, for Treatment of Alzheimer's Disease and Other Tauopathies
- Passive immunization with phospho-tau antibodies reduces tau pathology and functional deficits in two distinct mouse tauopathy models
- Increased brain penetration and potency of a therapeutic antibody using a monovalent molecular shuttle