Background Evidence is emerging that subtle language decline an early indicator of Alzheimer’s disease (AD). This study assessed change in semantic and letter fluency individuals with subjective cognitive (SCD), examined whether trajectories differed between without amyloid-beta (Aβ)-pathology. Method Longitudinal data from 437 the memory clinic-based Amsterdam Dementia Cohort were included (Ag...

Amyloid-β (Aβ) pathology is known to promote chronic inflammatory responses in the brain. It was thought previously that Aβ is only associated with Alzheimer's disease and Down syndrome. However, studies have shown its involvement in many other neurological disorders. The role of astrocytes in handling the excess levels of Aβ has been highlighted in the literature. Astrocytes have a distinctive...

Amyloid oligomers have emerged as the most toxic species of amyloid-β (Aβ). This hypothesis might explain the lack of correlation between amyloid plaques and memory impairment or cellular dysfunction. However, despite the numerous published research articles supporting the critical role Aβ oligomers in synaptic dysfunction and cell death, the exact definition and mechanism of amyloid oligomers ...

β-amyloid peptides (Aβ) are generated in intracellular compartments of neurons and secreted to form cytotoxic fibrils plaques. Dysfunctional membrane trafficking contributes aberrant Aβ production Alzheimer's disease. Endosomes represent one the major sites for recently Golgi has re-emerged also as a location amyloid precursor protein (APP) processing production. Based on recent findings, here ...

Alzheimer's disease is associated with a disruption of amyloid β (Aβ) homeostasis, resulting in the accumulation and subsequent deposition of Aβ peptides within the brain. The peroxisome proliferator-activated receptor-γ (PPARγ) is a ligand-activated nuclear receptor that acts in a coupled metabolic cycle with Liver X Receptors (LXRs) to increase brain apolipoprotein E (apoE) levels. apoE funct...

Cerebral accumulation of amyloid β-protein (Aβ) is thought to play a key role in the molecular pathology of Alzheimer's disease (AD). Three secretases (β-, γ-, and α-secretase) are proteases that control the production of Aβ from amyloid precursor protein. Increasing evidence suggests that cholesterol-rich membrane microdomains termed 'lipid rafts' are involved in the biogenesis and accumulatio...

The accumulation of amyloid-β (Aβ) as amyloid fibrils and toxic oligomers is an important step in the development of Alzheimer's disease (AD). However, there are numerous potentially toxic oligomers and little is known about their neurological effects when generated in the living brain. Here we show that Aβ oligomers can be assigned to one of at least two classes (type 1 and type 2) based on th...

Accumulation of amyloid β-peptide (Aβ) in the brain and its deposition into plaques is currently thought to be one of the key pathological features in Alzheimer’s disease (AD), and lead to neuronal dysfunction or neuronal death and cognitive impairment. However, the mechanisms how the Aβ exerts its effects neurobiologically remain elusive. Transgenic mice co-expressing mutated human amyloid pre...

Alzheimer’s disease (AD) is a severe neurodegenerative disorder characterized by β-amyloid (Aβ) plaques, neurofibrillary tangles, neuronal death, progressive cognitive impairment and memory loss. β-amyloid peptides (Aβ) are major compositions of so-called senile plaques, which are hallmarks of AD and contribute to AD progression. Therefore, it is important to discover therapeutics against Aβ-in...

Primary pathologies including amyloid-β (Aβ) plaques and neurofibrillary tangles (NFT) develop many years before the onset of dementia symptoms in Alzheimer's disease (AD). Age-related small vessel disease (SVD) is common in elderly subjects and may contribute to the clinical syndrome of AD. Each type of pathology shows a specific spatio-temporal sequence of spreading in the brain. Here, we rev...