Strong genetic evidence supports an imbalance between production and clearance of
amyloid β-protein (Aβ) in people with Alzheimer disease (AD). Microglia that are potentially …

The key pathological hallmarks—extracellular plaques and intracellular neurofibrillary
tangles (NFT)—described by Alois Alzheimer in his seminal 1907 article are still central to …

The history of Alzheimer's disease (AD) started in 1907, but we needed to wait until the end
of the century to identify the components of pathological hallmarks and genetic subtypes and …

Excitatory glutamatergic neurotransmission via N-methyl-d-aspartate receptor (NMDAR) is
critical for synaptic plasticity and survival of neurons. However, excessive NMDAR activity …

Nucleation of new peptide and protein aggregates on the surfaces of amyloid fibrils of the
same peptide or protein has emerged in the past two decades as a major pathway for both …

Background Amyloid protein precursor (APP), presenilin-1 (PSEN1), and presenilin-2
(PSEN2) mutations cause autosomal dominant forms of early-onset Alzheimer disease (AD …

In 2021, aducanumab, an immunotherapy targeting amyloid-β, was approved for
Alzheimer's disease (AD) by the US Food and Drug Administration thanks to positive results …

The risk of Alzheimer disease (AD) increases with age, family history and informative genetic
variants. Sadly, there is still no cure or means of prevention. As in other complex diseases …

Alzheimer's disease (AD) is the most common age-related neurodegenerative disorder that
is characterized by amyloid β-protein deposition in senile plaques, neurofibrillary tangles …

INTRODUCTION Alzheimer's disease (AD) is characterized by amyloid plaques in the brains
of patients. The primary components of amyloid plaques are β-amyloid peptides (Aβs) …