![Loading...](https://link.springer.com/static/c4a417b97a76cc2980e3c25e2271af3129e08bbe/images/pdf-preview/spacer.gif)
-
Article
Open AccessSpecific Mutations in the Cholesterol-Binding Site of APP Alter Its Processing and Favor the Production of Shorter, Less Toxic Aβ Peptides
Excess brain cholesterol is strongly implicated in the pathogenesis of Alzheimer’s disease (AD). Here we evaluated how the presence of a cholesterol-binding site (CBS) in the transmembrane and juxtamembrane re...
-
Article
Open AccessQuantification of SNAP-25 with mass spectrometry and Simoa: a method comparison in Alzheimer’s disease
Synaptic dysfunction and degeneration are central to Alzheimer’s disease (AD) and have been found to correlate strongly with cognitive decline. Thus, studying cerebrospinal fluid (CSF) biomarkers reflecting sy...
-
Article
Open AccessPrediction of Outcome After Endovascular Embolectomy in Anterior Circulation Stroke Using Biomarkers
Stroke is a major public health problem that can cause a long-term disability or death due to brain damage. Serious stroke is frequently caused by a large vessel occlusion in the anterior circulation, which sh...
-
Article
Open AccessNeurofilaments can differentiate ALS subgroups and ALS from common diagnostic mimics
Delayed diagnosis and misdiagnosis are frequent in people with amyotrophic lateral sclerosis (ALS), the most common form of motor neuron disease (MND). Neurofilament light chain (NFL) and phosphorylated neurof...
-
Article
Correction: Patient-specific Alzheimer-like pathology in trisomy 21 cerebral organoids reveals BACE2 as a gene dose-sensitive AD suppressor in human brain
-
Article
Open AccessPatient-specific Alzheimer-like pathology in trisomy 21 cerebral organoids reveals BACE2 as a gene dose-sensitive AD suppressor in human brain
A population of more than six million people worldwide at high risk of Alzheimer’s disease (AD) are those with Down Syndrome (DS, caused by trisomy 21 (T21)), 70% of whom develop dementia during lifetime, caus...
-
Article
Open AccessPredicting progression and cognitive decline in amyloid-positive patients with Alzheimer’s disease
In Alzheimer’s disease, amyloid- β (A β) peptides aggregate in the lowering CSF amyloid levels - a key pathological hallmark of the disease. However, lowered CSF amyloid levels may also be present in cognitively ...
-
Article
Open AccessLumbar and ventricular CSF concentrations of extracellular matrix proteins before and after shunt surgery in idiopathic normal pressure hydrocephalus
Idiopathic normal pressure hydrocephalus (iNPH) is a reversible CNS disease characterized by disturbed cerebrospinal fluid (CSF) dynamics. Changes in the extracellular matrix (ECM) composition might be involve...
-
Article
Open AccessA multifactorial model of pathology for age of onset heterogeneity in familial Alzheimer’s disease
Presenilin-1 (PSEN1) mutations cause familial Alzheimer’s disease (FAD) characterized by early age of onset (AoO). Examination of a large kindred harboring the PSEN1-E280A mutation reveals a range of AoO spann...
-
Article
Open AccessFamilial Alzheimer’s disease patient-derived neurons reveal distinct mutation-specific effects on amyloid beta
Familial Alzheimer’s disease (fAD) mutations alter amyloid precursor protein (APP) cleavage by γ-secretase, increasing the proportion of longer amyloidogenic amyloid-β (Aβ) peptides. Using five control induced...
-
Article
Open AccessDynamics of cerebrospinal fluid levels of matrix metalloproteinases in human traumatic brain injury
Matrix metalloproteinases (MMPs) are extracellular enzymes involved in the degradation of extracellular matrix (ECM) proteins. Increased expression of MMPs have been described in traumatic brain injury (TBI) a...
-
Article
Open AccessPerspectives in fluid biomarkers in neurodegeneration from the 2019 biomarkers in neurodegenerative diseases course—a joint PhD student course at University College London and University of Gothenburg
Until relatively recently, a diagnosis of probable Alzheimer’s disease (AD) and other neurodegenerative disorders was principally based on clinical presentation, with post-mortem examination remaining a gold s...
-
Article
Open AccessNovel tau fragments in cerebrospinal fluid: relation to tangle pathology and cognitive decline in Alzheimer’s disease
Tau is an axonal microtubule-binding protein. Tau pathology in brain and increased tau concentration in the cerebrospinal fluid (CSF) are hallmarks of Alzheimer’s disease (AD). Most of tau in CSF is present as...
-
Article
Open AccessThe intact postsynaptic protein neurogranin is reduced in brain tissue from patients with familial and sporadic Alzheimer’s disease
Synaptic degeneration and neuronal loss are early events in Alzheimer’s disease (AD), occurring long before symptom onset, thus making synaptic biomarkers relevant for enabling early diagnosis. The postsynapti...
-
Article
Open AccessCerebrospinal fluid neurogranin concentration in neurodegeneration: relation to clinical phenotypes and neuropathology
Neurogranin (Ng) is a post-synaptic protein that previously has been shown to be a biomarker for synaptic function when measured in cerebrospinal fluid (CSF). The CSF concentration of Ng is increased in Alzhei...
-
Article
Open AccessAlzheimer-associated cerebrospinal fluid fragments of neurogranin are generated by Calpain-1 and prolyl endopeptidase
Neurogranin (Ng) is a small 7.6 kDa postsynaptic protein that has been detected at elevated concentrations in cerebrospinal fluid (CSF) of patients with Alzheimer’s disease (AD), both as a full-length molecule...
-
Article
Open AccessThe presubiculum is preserved from neurodegenerative changes in Alzheimer’s disease
In the majority of affected brain regions the pathological hallmarks of Alzheimer’s disease (AD) are β-amyloid (Aβ) deposits in the form of diffuse and neuritic plaques, tau pathology in the form of neurofibri...
-
Article
Open AccessEx vivo 18O-labeling mass spectrometry identifies a peripheral amyloid β clearance pathway
Proteolytic degradation of amyloid β (Aβ) peptides has been intensely studied due to the central role of Aβ in Alzheimer’s disease (AD) pathogenesis. While several enzymes have been shown to degrade Aβ peptide...
-
Article
Open AccessAmyloid precursor protein expression and processing are differentially regulated during cortical neuron differentiation
Amyloid precursor protein (APP) and its cleavage product amyloid β (Aβ) have been thoroughly studied in Alzheimer’s disease. However, APP also appears to be important for neuronal development. Differentiation ...
-
Article
Open AccessA single dose of the γ-secretase inhibitor semagacestat alters the cerebrospinal fluid peptidome in humans
In Alzheimer’s disease, beta-amyloid peptides in the brain aggregate into toxic oligomers and plaques, a process which is associated with neuronal degeneration, memory loss, and cognitive decline. One therapeu...