Aggregation of amyloid-β (Aβ) as toxic oligomers and amyloid plaques within the brain appears to be the pathogenic event that initiates Alzheimer's disease (AD) lesions. One therapeutic strategy has been to reduce Aβ levels to limit its accumulation. Activation of certain neurotransmitter receptors can regulate Aβ metabolism. We assessed the ability of serotonin signaling to alter brain Aβ leve...

Amyloid accumulation in the brain of Alzheimer's patients results from altered processing of the 39- to 43-amino acid amyloid β protein (Aβ). The mechanisms for the elevated amyloid (Aβ(1-42)) are considered to be over-expression of the amyloid precursor protein (APP), enhanced cleavage of APP to Aβ, and decreased clearance of Aβ from the central nervous system (CNS). We report herein studies o...

Amyloid-β (Aβ) peptide deposition, hyperphosphorylated tau proteins, reactive astrocytes, high levels of metal ions, and upregulated monoamine oxidases are considered to be the primary pathological markers Alzheimer’s disease (AD). Among them, Aβ deposition or plaques, is regarded as initial factor in pathogenesis AD a critical hallmark AD. This review highlights recently Aβ-specific fluorescen...

Alzheimer's disease (AD) is marked by the presence of extracellular amyloid beta (Aβ) plaques, intracellular neurofibrillary tangles (NFTs) and gliosis, activated glial cells, in the brain. It is thought that Aβ plaques trigger NFT formation, neuronal cell death, neuroinflammation and gliosis and, ultimately, cognitive impairment. There are increased numbers of reactive astrocytes in AD, which ...

BACKGROUND Cistanche tubulosa (Schenk) R. Wight (CT) is commonly used to treat forgetfulness by traditional Chinese physicians. This study presents the ameliorating effects of CT extract which was quantified with three phenylpropanoid glycosides in Alzheimer's disease (AD)-like rat model. METHODS Amyloid β peptide 1-42 (Aβ 1-42) intracisternally infused to rats by osmotic pump (Alzet 2002) wa...

It has long been assumed that β-amyloid (Aβ) had to assemble into fibrillar amyloid plaques to exert its neurotoxic effects in Alzheimer disease. An alternative hypothesis is that soluble oligomers ofAβ play a much larger role in neuronal damage than the insoluble component. We have tested these competing hypotheses in vivo by studying the clinicopathologic correlates of oligomeric Aβ species a...

Alzheimer’s Disease (AD) is a progressive neurological disorder associated with cognitive and memory deficits. Accumulation of amyloid beta (Aβ) plaques is one of the major causes of AD. Therefore, inhibition of the plaque formation has been aimed to play a preventive role in the disease. Lavender, through some neuroprotective roles such as antioxidant effects, is known to be an effective c...

Amyloid beta (Aβ) is a peptide derived from processing of the membrane bound amyloid precursor protein and is a main constituent in amyloid plaques in Alzheimer's disease (AD). The excess Aβ in AD brain may be caused by altered Aβ metabolism, including reduced enzymatic degradation. Our previous enzymatic study of Aβ degradation revealed that intracellular enzymes produced several truncated Aβ ...

Alzheimer's disease (AD) etiological studies suggest that an elevation in amyloid-β peptides (Aβ) level contributes to aggregations of the peptide and subsequent development of the disease. The major constituent of these amyloid peptides is the 1 to 40-42 residue peptide (Aβ(40-42)) derived from amyloid protein precursor (APP). Most likely, reducing Aβ levels in the brain may block both its agg...

The amyloid-beta (Aβ) hypothesis that dyshomeostasis between Aβ production and clearance is a very early, key molecular factor in the etiology of Alzheimer's disease (AD) has been proposed and examined in the AD research field. Scientists have focused on seeking natural products or drugs to influence the dynamic equilibrium of Aβ, targeting production and clearance of Aβ. There is emerging evid...