Peptides for Alzheimer's Research

Alzheimers

Peptides for Alzheimer's Disease Research

About Alzheimer's Disease

Alzheimer's Disease (AD) is a neurodegenerative disorder that progressively damages brain cells, leading to memory loss, cognitive decline, and eventually death. Most commonly diagnosed after the age of 65, Alzheimer's also affects younger individuals, with about 5% of patients suffering from early-onset Alzheimer's Disease. Despite extensive research, the exact mechanisms causing Alzheimer's remain unclear. However, several hypotheses exist to explain its development.

One hypothesis focuses on the hyperphosphorylation of tau protein, while another centers around the buildup of amyloid plaques in the brain. These plaques are primarily composed of amyloid beta (Aβ) peptides, which are also implicated in other protein misfolding diseases, such as prion disorders. Understanding the role of peptides in Alzheimer's disease is critical to advancing potential treatments and therapies.

Role of Amyloid Beta Peptide in Alzheimer's Disease

Amyloid Beta (Aβ), also known as Beta Amyloid A4, plays a pivotal role in Alzheimer's disease pathology:

Beta Amyloid A4 peptide (also referred to as Aβ, Abeta, Amyloid Beta) serves several functions in a healthy brain, such as activating kinases and regulating cholesterol transport.

The accumulation of amyloid plaques, primarily composed of Aβ peptides, is a key pathological hallmark of Alzheimer's disease.

Aβ peptides arise from the amyloid precursor protein (APP), undergoing proteolytic processing through β- and γ-secretases.

These peptides vary in length (up to 43 amino acids), and certain isoforms, particularly Aβ(1-42) and Aβ(1-43), are highly prone to aggregation.

A pathological increase in β/γ-secretase activities and a reduced clearance rate of Aβ peptides can result in their accumulation in the brain, contributing to the formation of toxic oligomers, fibrils, and plaques.

These amyloid beta aggregates disturb the neuronal network and are believed to exert neurotoxic effects, leading to the cognitive and behavioral impairments observed in Alzheimer's patients.

Despite years of research, the exact biochemical pathways driving the neurotoxic effects of Aβ peptides are still not fully understood, making Alzheimer's disease research a critical area of focus for peptide scientists.

JPT's Peptide Tools for Alzheimer's Research

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Custom Peptide Synthesis

A21G-Beta-Amyloid (1-42) HFIP treated

US$620.10

A2T-Beta-Amyloid (1-42) HFIP treated

US$208.00

A2V-Beta-Amyloid (1-40) HFIP treated

US$577.20

A2V-Beta-Amyloid (1-42) HFIP treated

Beta-Amyloid (1-37) HFIP treated

Beta-Amyloid (1-38) HFIP treated

Beta-Amyloid (1-40) Scrambled HFIP treated

US$193.70

Beta-Amyloid (1-40)-Lys(Biotinoyl) HFIP

US$270.40

Beta-Amyloid (1-42) HFIP treated

Amyloid Beta Peptides for Alzheimer's Research

At JPT, we provide a comprehensive collection of Amyloid Beta (Aβ) peptides for studying Alzheimer's disease. Our peptide portfolio includes both various lengths of Aβ peptides and point-mutated versions of Aβ(1-42), known to be associated with familial forms of Alzheimer's. These peptides are delivered as HFIP-films (hexafluoroisopropanol) to eliminate unwanted secondary structures and any pre-existing oligomers or polymers, ensuring maximum experimental accuracy.

Researchers focusing on Alzheimer’s peptide studies can benefit from the high purity and customization of these peptides for in vitro and in vivo Alzheimer's research.

Custom Peptide Synthesis for Alzheimer's Disease Studies

Custom peptides synthesis for Alzheimer's play an essential role in advancing Alzheimer's studies by enabling scientists to create specific peptides for their unique research needs. JPT is renowned for our Custom Peptide Synthesis services, offering:

Over 99% success rate in peptide synthesis, optimizing the process for each specific peptide sequence.

Tailored solutions for Alzheimer's peptide research, with strict quality control and regulated processes to ensure consistency and accuracy.

A dedicated team of peptide experts, ensuring your peptides meet the highest standards required for Alzheimer’s disease studies.

Whether you are looking for standard Aβ peptides or complex, modified peptides for Alzheimer's research, JPT’s synthesis services provide the best tools to accelerate your experiments.

References

Aβ-reactive T cell polyfunctionality response as a new biomarker for mild cognitive impairmentChio et al., Diagnosis, Assessment & Disease Monitoring (2025) Product used: A21G-Beta-Amyloid (1-42) HFIP treated, PepMix™ Human CMV (pp65)

Cerebrospinal fluid markers link to synaptic plasticity responses and Alzheimer’s disease genetic pathwaysKirsebom et al., Molecular Neurodegeneration (2025) Product used: SpikeTides L

The structure of amyloid-β (1–42) oligomers in membranemimetic environmentsKuryshev et al., Spectrochimica Acta Part A: Molecular and Biomolecular Spectroscopy (2025) Product used: Amyloid Beta, V18*Aβ42

Molecular interactions, structural effects, and binding affinities between silver ions (Ag+) and amyloid beta (Aβ) peptidesLakela et al., Scientific Reports (2025) - PMID: 39948350

Novel 6-hydroxybenzothiazol-2-carboxamides as potent and selective monoamine oxidase B inhibitors endowed with neuroprotective activityAl-Saad et al., European Journal of Medicinal Chemistry (2024) - PMID: 38490063

Generation of nanobodies with conformational specificity for tau oligomers that recognize tau aggregates from human Alzheimer's disease samplesMcArthur et al., Biomaterials Science (2024) - PMID: 39434503Product used: PepSpots Peptides on Cellulose

β-amyloid monomer scavenging by an anticalin protein prevents neuronal hyperactivity in mouse models of Alzheimer’s Disease

Residue‑specifc binding of Ni(II) ions infuences the structure and aggregation of amyloid beta (Aβ) peptidesBerntsson et al., Scientific Reports (2023) - PMID: 36849796

Domino-like effect of C112R mutation on ApoE4 aggregation and its reduction by Alzheimer’s Disease drug candidateNemergut et al., Molecular Neugodenegeration (2023) - PMID: 37280636Product used: SpikeTides L

Protein Expression of Amino Acid Transporters Is Altered in Isolated Cerebral Microvessels of 5xFAD Mouse Model of Alzheimer’s DiseasePuris et al., Molecular Neurobiology (2023) - PMID: 36367657Product used: SpikeTides TQL

Cerebral organoids derived from patients with Alzheimer’s disease with PSEN1/2 mutations have defective tissue patterning and altered developmentVanova et al., Cell Reports (2023) - PMID: 37864790Product used: SpikeTides L

Systemic inflammation elevates cytosolic prolyl oligopeptidase protein expression but not peptidase activity in the cerebral cortices of familial Alzheimer`s disease modeling micePuris et al., Brain Disorders (2022)

Enhanced ion mobility resolution of Abeta isomers from human brain using high‑resolution demultiplexing softwareMukherjee et al., Analytical and Bioanalytical Chemistry (2022)

A novel D-amino acid peptide with therapeutic potential (ISAD1) inhibits aggregation of neurotoxic disease-relevant mutant Tau and prevents Tau toxicity in vitroIsabelle Aillaud et al., Alzheimer's Research & Therapy, (2022)

A Comparative Study of the Effects of Aducanumab and Scanning Ultrasound on Amyloid Plaques and Behavior in the APP23 Mouse Model of Alzheimer DiseaseGerhard Leinenga et al., bioRxiv (2020) - PMID: n.a.

Citrullination of Amyloid-β Peptides in Alzheimer’s DiseaseSoumya Mukherjee et al., ACS Chem Neurosci, (2021)

Lithium Ions Display Weak Interaction With Amyloid-Beta (Aβ) Peptides And Have Minor Effects On Their AggregationElina Berntsson et al., bioRxiv (2020) - PMID: n.a.

Analyzing Microglial‑Associated Aβ in Alzheimer’s Disease Transgenic Mice With a Novel Mid‑Domain Aβ‑AntibodyKristi Henjum et al., Scientific Reports (2020) - PMID: 32601313

In Situ Structural Characterization of Early Amyloid Aggregates in Alzheimer’s Disease Transgenic Mice And Octodon DegusNúria Benseny-Cases et al., Scientific Reports (2020) - PMID: 32246090

Long‑term cafeine treatment of Alzheimer mouse models ameliorates behavioural defcits and neuron loss and promotes cellular and molecular markers of neurogenesisMartina Stazi et al., Cellular and Molecular Life Science, (2021)

Alzheimer's Disease Phenotype or Inflammatory Insult Does Not Alter Function of L-Type Amino Acid Transporter 1 in Mouse Blood-Brain Barrier and Primary AstrocytesGynther et al., Pharmaceutical Research (2019)

Poly(propylene imine) Dendrimers With Histidine-Maltose Shell as Novel Type of Nanoparticles for Synapse and Memory ProtectionAso et al., Nanomedicine: Nanotechnology, Biology and Medicine (2019)

The Metalloprotease ADAMTS4 Generates N-truncated Aβ4-x Species and Marks Oligodendrocytes as a Source of Amyloidogenic Peptides in Alzheimer's DiseaseWalter et al., Acta Neuropathologica (2018)

Amyloid-peptide β 42 Enhances the Oligomerization and Neurotoxicity of apoE4: The C-terminal Residues Leu279, Lys282 and Gln284 Modulate the Structural and Functional Properties of apoE4 IDafnis et al., Neuroscience (2018)

Synchrotron-Based µFTIR Study on the Effect of Alzheimer´s Aβ Amorphous and Fibrillar Aggregates on PC12 CellsBenseny-Cases et al., Analytical Chemistry (2018)

Neprilysin Deficiency Alters the Neuropathological and Behavioral Phenotype in the 5XFAD Mouse Model of Alzheimer's DiseaseHuettenrauch et al., J Alzheimers Dis. (2014) - PMID: 25408216

Monoclonal Antibodies Against Ab42 Fibrils Distinguish Multiple Aggregation State Polymorphisms in vitro and in Alzheimer's Disease BrainHatami et al., J. Biol. Chem. (2014) - PMID: 25281743

The Alzheimer Disease Protective Mutation A2T Modulates Kinetic and Thermodynamic Properties of Amyloid-β (Aβ) AggregationBenilova et al., J. Biol. Chem. (2014) - PMID: 25253695

Molecular Basis for Increased Risk for Late-onset Alzheimer Disease Due to the Naturally Occurring L28P Mutation in Apolipoprotein E4Argyri et al., J. Biol. Chem. (2014) - PMID: 24644280

Effect of Poly(propylene imine) Glycodendrimers on β-Amyloid Aggregation in Vitro and in APP/PS1 Transgenic Mice, as a Model of Brain Amyloid Deposition and Alzheimer’s DiseaseKlementieva et al., Biomacromolecules (2013) - PMID: 24004423

Nanoparticulate Flurbiprofen Reduces Amyloid-β42 Generation in an in Vitro Blood-Brain Barrier ModelMeister et al., Alzheimers Research & Therapy (2013) - PMID: 24280275

The Amyloid-β Oligomer Count in Cerebrospinal Fluid is a Biomarker for Alzheimer's DiseaseWang-Dietrich et al., Journal of Alzheimer's Disease (2013) - PMID: 23313925

DNA Beta-Amyloid1-42 Trimer Immunization for Alzheimer Disease in a Wild-Type Mouse ModelLambracht-Washington et al., JAMA, (2009) - PMID: 19861672

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