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.
-
Cleavage of the amyloid precursor protein's (APP) transmembrane domain (TMD) by γ-secretase is a crucial step in the aetiology of Alzheimer's Disease (AD).
-
Several lines of evidence have shown that defects in the endo-lysosomal autophagy degradation pathway and the ubiquitin-proteasome system play a role in Alzheimer's Disease (AD) pathogenesis and pathophysiology.
-
The presenilin (PS) proteins exert a crucial role in the pathogenesis of Alzheimer disease (AD) by mediating the intramembranous cleavage of amyloid precursor protein (APP) and the generation of amyloid β-protein (Aβ).
-
Alzheimer's disease (AD) is characterized by the formation of extracellular amyloid plaques containing the amyloid β-protein (Aβ) within the parenchyma of the brain.
-
Alzheimer's disease (AD) is characterized by the coexistence of amyloid-β (Aβ) plaques and tau-based neurofibrillary tangles.
-
Dendritic spines are small, thin, specialized protrusions from neuronal dendrites, primarily localized in the excitatory synapses.
-
Efforts to develop effective disease-modifying treatments for Alzheimer's disease (AD) have mostly targeted the amyloid β (Aβ) protein; however, there has recently been increased interest in other targets including phosphorylated tau and other forms of tau.
-
39/100
In normal physiological condition, the maintenance of cellular proteostasis is a prerequisite for cell growth, functioning, adapting to changing micro-environments, and responding to extracellular stress.
-
Protein homeostasis (proteostasis) refers to the ability of cells to preserve the correct balance between protein synthesis, folding and degradation.
-
39/100
Dozens of genes have been implicated in late onset Alzheimer's disease (AD) risk, but none has a defined mechanism of action in neurons.
-
39/100
Imbalance of neuronal proteostasis associated with misfolding and aggregation of Tau protein is a common neurodegenerative feature in Alzheimer's disease (AD) and other Tauopathies.
-
Delivering drugs and agents to the brain is a huge challenge, especially for chronic neurodegenerative disorders, such as Alzheimer's disease (AD).
-
Age is the common risk factor for both neurodegenerative and neuromuscular diseases.
-
Mutations in fused in sarcoma (Fus) cause familial amyotrophic lateral sclerosis (ALS) and occasionally frontotemporal dementia.
-
The term proteostasis reflects the fine-tuned balance of cellular protein levels, mediated through a vast network of biochemical pathways.
-
Tau, the main component of the neurofibrillary tangles (NFTs), is an attractive target for immunotherapy in Alzheimer's disease (AD) and other tauopathies.
-
Alzheimer's disease (AD) is a heterogeneous neurodegenerative disorder and represents the most common form of dementia in the elderly.
-
Klotho, encoded by the KL gene, is a single-pass transmembrane protein and a circulating factor that plays a key role in cellular metabolism and body homeostasis and has been associated with age-related diseases.
-
Alzheimer's disease (AD) is a progressive neurodegenerative disease with no clinically accepted treatment to cure or halt its progression.
-
Alzheimer's disease (AD) is emerging as a synaptopathology driven by metaplasticity.
-
Neutral sphingomyelinase smpd3 is most abundantly expressed in neurons of brain.
-
The ubiquitin-proteasomal-system (UPS) and the autophagy-lysosomal-system (ALS) are both highly susceptible for disturbances leading to the accumulation of cellular damage.
-
Early-stage Alzheimer's disease is characterized by the loss of dendritic spines in the neocortex of the brain.
-
39/100
The most common neurodegenerative diseases, such as Alzheimer's, Parkinson's, and amyotrophic lateral sclerosis, are all protein-misfolding diseases and are characterized by the presence of disease-specific protein aggregates in affected neuronal cells.
-
Synaptic plasticity is a cellular process involved in learning and memory whose alteration in its two main forms (Long Term Depression (LTD) and Long Term Potentiation (LTP)), is observed in most brain pathologies, including neurodegenerative disorders such as Alzheimer's disease (AD).
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.
- Mitotic activation: a convergent mechanism for a cohort of neurodegenerative diseases
- beta-Amyloid(1-42) binds to alpha7 nicotinic acetylcholine receptor with high affinity. Implications for Alzheimer's disease pathology
- Neuronal pentraxin 1 negatively regulates excitatory synapse density and synaptic plasticity
- Associations of Neprilysin Activity in CSF with Biomarkers for Alzheimer's Disease
- Ageing and Parkinson's disease: why is advancing age the biggest risk factor?
- Rab11-exosome biogenesis regulators mediate Aβ-induced intercellular propagation of endolysosomal trafficking defects and neurodegeneration
- Lewy Bodies Contain Altered α-Synuclein in Brains of Many Familial Alzheimer's Disease Patients with Mutations in Presenilin and Amyloid Precursor Protein Genes
- Advances in progressive supranuclear palsy: new diagnostic criteria, biomarkers, and therapeutic approaches
- Tau phosphorylation at Alzheimer's disease biomarker sites impairs its cleavage by lysosomal proteases
- Modulation of Tau Pathology in Alzheimer's Disease by Dietary Bioactive Compounds