Hayder Amin
Plasticity Models for Aging and Neurodegeneration
Dr. Hayder Amin
Group Leader
Tatzberg 41
01307  Dresden

 +49 351 210 463-602

Areas of investigation/research focus

The laboratory is interested in understanding the interplay between molecular and cellular processes and functional plasticity consequences in neurophysiological states, aging and neurodegenerative disorders.
We use multidisciplinary experimental and computational approaches to examine multiple forms of plasticity as changes in the electrical and chemical signals in large-scale networks at single-neuronal details.

The adult brain is a uniquely plastic organ capable of generating new neurons throughout life to modify its structure and function to continuously learn and adapt to changes in everyday experience and environmental demands. These activity-dependent plasticity changes can be ‘functional’, where neurons, adjust their electrophysiological properties. They can also be ‘molecular’, involving the regulation of particular gene expression patterns that are essential for the formation, maturation, and regulation of synaptic strength in those same neurons.

  • But how are functional and molecular processes of plasticity interrelated?
  • What is the functional role of newly-generated neurons in the adult brain?
  • What is the mechanism underlying the integration of these neurons into a resident network?
  • Importantly, how can the brain exploit these new neurons to stall the consequence demands of aging and neurodegeneration?

To address these questions, linking morphological, electrophysiological, and transcriptomic data at a single neuron in a large-scale network is essential but has lagged behind due to the lack of multimodal and multiscale techniques. Our laboratory aims to circumvent these challenges by using advanced molecular and cellular, electrophysiological, imaging and computation methodologies.

 more Infos


Our research themes  involve projects in the following areas:

1. Neurogenic-plasticity models for aging and neurodegeneration: from genes to spikes

We aim to characterize the activity-dependent adjustments (from genes to spiking networks) of newly-generated neurons for the recruitment and functional integration into diseased or aged neuronal ensembles.

2. E/I balanced networks for empowering neuronal coding and synaptic stability

We study the long-term plasticity of excitatory and inhibitory (E/I) synaptic drive. We investigate how balanced E/I regime confers robust, and high-dimensional neural codes and computational performance.

3. Engineering the brain-on-a-chip (microfluidic channels integrated with CMOS-MEAs)

We design and implement systemic microfluidic platform on CMOS-MEAs to allow modeling different brain cell types for fundamental research, disease modeling, and drug development.

4. Bottom-up computational modeling

Our integrative approach aims to create a bottom-up comprehensive network modeling to simulate multi-level experimental plasticity readouts (molecular, cellular and networks).

5. Biofunctionalized platform for neural interfaces

We develop biofunctionalization methods to grow neuronal networks in well-defined configuration to investigate cell-to-cell and cell-extracellular matrix interactions. These methods also aim to improve the neuron-electrode interface to enhance the quality of the recorded neural signals.

Diseases related to these fields of research:

  • Alzheimer’s disease (AD)
  • Amyloid-beta toxicity (Aβ)
  • Parkinson’s disease (PD)
  • Amyotrophic lateral sclerosis (ALS)

Techniques: We build sophisticated approaches to index various neuroscience challenges from genes to networks by using:

  • In-vitro HiPSC-derived neuronal cultures and ex-vivo transgenic mouse brain slices
  • High-resolution CMOS-MEAs
  • Calcium imaging
  • Patch-clamp recordings
  • Genome-wide transcriptome profiling
  • Opto-and-chemogenetic
  • Molecular and cellular techniques
  • Micro-/nanotechnology
  • Computational modeling

Key Publications

Amin H, Dipalo M, De Angelis F, Berdondini L. Biofunctionalized 3D nanopillar arrays fostering cell-guidance and promoting synapse stability and neuronal activity in networks. ACS Appl Mater Interfaces. 2018 Jan 01; 1-9 doi: 10.1021/acsami.8b00387
Amin H, Marinaro F, Tonelli DDP, Berdondini L. Developmental excitatory-to-inhibitory GABA-polarity switch is disrupted in 22q11.2 deletion syndrome: A potential target for clinical therapeutics. Sci Rep. 2017 Jan 01; 7:1-18. doi: 10.1038/s41598-017-15793-9
Amin H, Nieus T, Lonardoni D, Maccione A, Berdondini L. High-resolution bioelectrical imaging of Aβ-induced network dysfunction on CMOS-MEAs for neurotoxicity and rescue studies. Sci Rep. 2017 Jan 01; 7:2460. doi: 10.1038/s41598-017-02635-x
Amin H, Maccione A, Marinaro F, Zordan S, Nieus T, Berdondini L. Electrical responses and spontaneous activity of human iPS-derived neuronal networks characterized for 3-month culture with 4096-electrode arrays. Front Neurosci. 2016 Jan 01; 10:1-15. doi: 10.3389/fnins.2016.00121
Amin H, Maccione A, Zordan S, Nieus T, Berdondini L. High-density MEAs reveal lognormal firing patterns in neuronal networks for short and long term recordings. IEEE. 2015 Jan 01; :1000-1003. doi: 10.1109/NER.2015.7146795


Thursdays 1:30-4:30 pm

Patients +49 800-7799001

(free of charge)

Professionals +49 180-779900

(9 Cent/Min. German landline, mobile and out of Germany possibly more expensive)

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