AD – Evolution and pathological mechanism

Alzheimer’s Disease (AD) is a progressive and irrevocable neurodegenerative disease. It slowly affects brain tissue and provokes irrevocable motor and psychological functions loss.

AD mild symptoms usually first manifest in individuals as much as 8 years before they are officially diagnosed with the disease. Short-term memory loss, difficulty to accomplish complex tasks, problems with semantic memory and understanding are the most common of the pre-dementia symptoms.

Following those mild cognitive deficits, language deficit, motor dysfunction, agnosia and apraxia then confirm the diagnosis. 

AD doesn’t affect all individuals the same way and symptoms frequency and severity is evaluated on a case-by-case basis.

Alzheimer’s Disease patients’ brains suffer both a degeneration and inflammation process. At the extracellular level within the brain, Beta-amiloïd epeptide starts to accumulate and form what is characteristically referred to as “plaque”. At the same time, Tau protein accumulates inside brain cells and provoke the formation of neurofibrils. 

Progressively, a loss of neurons and synapsis in the cortex is observed, which causes the affected brain regions to retract (atrophia).

Evaluate your compound’s effect on Alzheimer’s models

Tg models for in vitro studies

Our member Neuroservice, CNS CRO specialized in in vitro electrophysiology, successfully showed that Tg mice display electrophysiological properties deficits compared to their wild type counterparts. As an expert in electrophysiological studies, Neuroservice can study your compound’s efficacy on such models. 

  • Slice electrophysiology on AD mice models
  • Electrophysiology on slice exposed to Beta-amyloid

iPSC-derived neurons from AD patients

  • Our expert platform Neuroservice is expert in characterizing, validating and performing pharmacological testing on all types of human iPSC-derived neurons.
    Thanks to commercially available iPSCs derived from AD patient donors, we can help you investigate your compound’s activity on human tissue in a condition approaching very closely the physiological condition.

in vivo models

Our member KEY-OBS, preclinical CNS CRO specialized in in vivo models of neurological disorders, has developed models simulating closely Alzheimer’s Disease symptoms.

  • Scopolamine -induced amnesia
  • Social memory / social recognition test
  • Memory deficit in Tg2576
  • Novel Object Recognition

Our member Motac, world-reknowned expert in Neurodegenerative disorders modelling, has developed several AD-specific rodent and non-human primate models:

  • NHP model for cognitive performances – aged animals are ideal for evaluating cognition-enhancing strategies
  • NHP Scopolamine model – model of memory failure in AD

Our member OptoPath, a rodent platform entirely dedicated to innovation in experimental psychopathology, provides behavioral test to assess impairments characteristic of AD:

  • Declarative memory behavioural test
  • Spatio-temporal memory assessment in maze

Please contact us for more information on our available AD models and assays.

Erwan BEZARD, PhD
CSO, AD/PD expert
MOTAC
Bruno BUISSON, PhD
Co-Founder, President & CSO
NEUROSERVICES-ALLIANCE
& NEUROSERVICE
Bob PETROSKI, PhD
Scientific liaison
NEUROSERVICES-ALLIANCE
Jeffrey HUBBARD, PhD
Head of Patch-Clamp laboratory
NEUROSERVICE
Jean-Charles BIZOT, PhD
CEO & Behavioral Pharmacologist
KEY-OBS
Fabrice TROVERO,PhD
GM & Behavioral Pharmacologist
KEY-OBS
Aline MARIGHETTO, PhD
Memory Deficits
OPTOPATH
Nora ABROUS, PhD
Memory Deficits & Neurogenesis
OPTOPATH