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Related Concept Videos

Alzheimer's Disease: Treatment01:22

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Alzheimer's Disease (AD), a neurodegenerative disorder, is pathologically identified by amyloid plaques and neurofibrillary tangles composed of tau protein. AD pharmacotherapy aims to manage cognitive symptoms, delay disease progression, and treat behavioral symptoms. The treatment is primarily symptomatic and palliative, with no definitive disease-modifying therapy available. Cholinesterase inhibitors, including donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne), are...
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Drugs affecting neurotransmitter synthesis can impact the adrenergic neuron and the synthesis of neurotransmitters. For example, α-methyltyrosine and carbidopa target specific enzymes involved in catecholamine synthesis. α-methyltyrosine inhibits the enzyme tyrosine hydroxylase, which converts tyrosine into dopamine. By blocking this enzyme, α-methyltyrosine reduces dopamine production and other catecholamines. Carbidopa, on the other hand, inhibits the enzyme dopa decarboxylase,...
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Amyloid Fibrils03:03

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Amyloid fibrils are aggregates of misfolded proteins.  Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils. 
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Certain drugs can affect how neurotransmitters called catecholamines, are released or taken back up in the adrenergic neuron. They can have different effects on the body's sympathetic transmission. Reserpine, a natural compound found in the Rauwolfia shrub, blocks a transporter called vesicular monoamine transporter (VMAT), which leads to a buildup of catecholamines in the cell and reduces sympathetic transmission. Another drug called guanethidine works in multiple ways, including blocking...
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Neurochemical transmission, the conduction of electrical impulses between neurons mediated by neurotransmitters, plays a vital role in various physiological processes. Autonomic drugs exert their effects by modulating neurotransmission within the autonomic nervous system. For instance, drugs such as hemicholinium block the precursor uptake necessary for synthesizing acetylcholine, an essential autonomic neurotransmitter. Following synthesis, neurotransmitters are stored in vesicles. Metyrosine...
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Related Experiment Video

Updated: Dec 20, 2025

Preparation of Oligomeric β-amyloid1-42 and Induction of Synaptic Plasticity Impairment on Hippocampal Slices
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Partial reduction of amyloid β production by β-secretase inhibitors does not decrease synaptic transmission.

Tugce Munise Satir1, Lotta Agholme2, Anna Karlsson3

  • 1Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, the Sahlgrenska Academy at the University of Gothenburg, S-415 30, Gothenburg, Sweden.

Alzheimer'S Research & Therapy
|May 28, 2020
PubMed
Summary
This summary is machine-generated.

Partial inhibition of beta-secretase (BACE) can reduce amyloid-beta (Aβ) generation without impairing synaptic function. This suggests moderate BACE inhibitor doses may be effective for Alzheimer's disease prevention.

Keywords:
Alzheimer’s diseaseAmyloid betaBACE inhibitionBeta-secretaseSynaptic transmission

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Area of Science:

  • Neuroscience
  • Pharmacology
  • Biochemistry

Background:

  • Alzheimer's disease (AD) is characterized by cerebral amyloid-beta (Aβ) deposition, primarily Aβ42.
  • Beta-secretase (BACE) initiates amyloid precursor protein (APP) processing, making it a therapeutic target.
  • Previous BACE inhibitor trials failed, possibly due to late intervention or impaired synaptic function.

Purpose of the Study:

  • Investigate if partial BACE inhibition reduces Aβ generation without affecting synaptic transmission.
  • Mimic the protective effect of the Icelandic mutation in APP.

Main Methods:

  • Utilized an optical electrophysiology platform to monitor synaptic transmission in cultured rat neurons.
  • Treated neuronal cultures with three BACE inhibitors: BACE inhibitor IV, LY2886721, and lanabecestat.
  • Measured Aβ secretion into cell media.

Main Results:

  • All tested BACE inhibitors reduced synaptic transmission at high concentrations.
  • Low-dose BACE inhibition ( <50% Aβ reduction) did not impact synaptic transmission.

Conclusions:

  • Reducing Aβ production by up to 50% is achievable without synaptic dysfunction.
  • Suggests moderate central nervous system (CNS) exposure of BACE inhibitors for future AD prevention trials.
  • Aims to avoid synaptic side effects while targeting Aβ build-up.