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About neurodegenerative diseases

Neurodegenerative diseases (NDDs) likely share a common pathophysiological mechanism involving accumulation, propagation and deposition of aggregates comprised of soluble proteins, truncated peptides, and/or polyamines, all of which being abnormally misfolded. Under physiological conditions, neurons remove abnormal, altered or long-lived cellular proteins by various mechanisms such as molecular chaperone-mediated refolding, degradation by the ubiquitin–proteasome system (UPS) proteases or peptidases, autophagy and sequestration into microtubule-dependent aggresomes. Under non-physiological conditions such as pathological oxidative stress, soluble native or non-native polypeptides may self-assemble, polymerize and form intracellular inclusions.

Among neurodegenerative diseases, AlzProtect focuses on tauopathies where neuronal degeneration is a consequence of the abnormal aggregation of hyperphosphorylated tau proteins. Currently, the company develops drug candidates for the treatment of Alzheimer's disease and orphan disease Progressive Supranuclear Palsy (PSP).

About Alzheimer’s disease

Alzheimer’s Disease (AD) is the most common form of dementia. First described in 1906 by Dr. Aloïs Alzheimer, this disease is characterized by a progressive and irreversible destruction of the nerve cells (neurons) that are localized in two specific areas of the brain : the hippocampus  and the associative cortex.

Neuronal degeneration and subsequent destruction first lead to memory deficits and then to  alteration of personality, language and behavior up to a complete autonomy loss and dementia. In late stages of the disease, all cortex areas and sub-cortical nuclei exhibit two different types of lesion: amyloid plaques and neurofibrillary tangles. 

In the course of neuronal degeneration,  the microtubule network is transformed into filaments composed of abnormal Tau proteins. Concomitantly, amyloid plaques are formed due to the aggregation of  extracellular Amyloid-beta peptide. This peptide has a low solubility and originates from an abnormal processing of the Amyloid Precursor Protein (APP). 

Since Dr Aloïs Alzheimer first observations, researchers have gained a better understanding of the changes occurring in the brain and the cognitive deficiency hallmarks of the disease. They have also identified several genes associated to the (hereditary) familial forms of the disease which affect only 2% of patients. Despite major research efforts, the exact causes and mechanisms of the disease remain to be fully elucidated.

Alzheimer’s disease is the 4th cause of death in adults and equally affects both genders. The majority of patients are over 65 but onset of the disease could start at the age of 50 or even 40 in patients suffering from the (hereditary) familial form of the disease. 

Alzheimer’s disease Forum: www.alzforum.org
French Alzheimer Patients’ Association: www.francealzheimer.org                                                          
Alzheimer Europe : www.alzheimer-europe.org

About Progressive Supranuclear Palsy

Progressive Supranuclear Palsy (PSP or Steele-Richardson-Olszewski syndrome) is a progressive neurodegenerative disorder. This clinical syndrome is characterized by a supranuclear palsy, postural instability, progressive rigidity and mild dementia1. Neuropathologically, PSP is defined by neuronal loss, gliosis with stufted astrocytes and accumulation of tau-immunoreactive neurofibrillary tangles (NFTs) in the basal ganglia, brainstem and cerebellar nuclei2

PSP is most often diagnosed in patients who are in their 60’s. Within the E.U., the disease affects approximately 30,000 patients with a prevalence estimated at 1/16,600. 

Early symptoms include loss of balance, stiffness of the neck, and unexpected falls (often backwards).  As the disease progresses, these symptoms worsen and difficulties with eye movements, speech, swallowing, and thinking occur. Other nonspecific symptoms of PSP occur, such as slowed movements or behavioral or cognitive changes. PSP is a rapidly progressing neurodegenerative disease leading to a progressive inability to move and poor prospects of long term survival (average of 6 years following onset of symptoms).

Currently, there are no FDA or EMA approved treatment for PSP. 

1 Williams DR, Lees AJ. Progressive supranuclear palsy: clinicopathological concepts and diagnostic challenges. Lancet      Neurol. 2009 Mar; 8(3):270-9.
2 Dickson DW, Kouri N, Murray ME, Josephs KA. Neuropathology of frontotemporal lobar degeneration-tau (FTLD-tau). J Mol Neurosci. 2011 Nov; 45(3):384-9.

PSP France : www.pspfrance.org                                                                                                                                   Cure PSP: www.psp.org
Movement Disorders Society: www.movementdisorders.org
Tau consortium : www.tauconsortium.org