Neurological disorders are increasingly being recognized as major causes of death and disability worldwide. A recent worldwide epidemiological study found the burden of neurological disorders, measured in terms of the absolute number of disability-adjusted life-years (DALYs), i.e., the sum of years of life lost and years lived with disability by age and sex, has increased for most neurological disorders in the last decade
[1]. Among common neurological disorders, Alzheimer’s disease (AD) and multiple sclerosis (MS) are associated with high-morbidity levels and health costs
[2,3][2][3]. To date, only symptomatic pharmacological treatments have been approved for the treatment of AD, including cholinesterase inhibitors and N-methyl-d-aspartate receptor antagonists, as the cornerstone of pharmacotherapy
[4]. The amyloid beta (Aβ) peptide is the main protein component of the extracellular space found in senile plaque in the brain parenchyma, and is involved in memory dysfunction in AD
[5,6][5][6]. Besides accumulation of Aβ peptide, other pathogenic hallmarks, such as neurofibrillary tangles, are responsible for the pathology of AD
[7]. MS is a chronic-autoimmune disease of the central nervous system (CNS) which is most common in young female patients. Its pathophysiological hallmark is the destruction of the myelin sheath, with axonal degeneration and neuronal cell death. Furthermore, pharmacological treatment in MS is not curative, and is based on three goals: treatment of exacerbations, slowing the disease’s progression with disease-modifying therapies (DMTs), and symptomatic therapies
[8]. Disease-modifying drugs have mostly failed as treatments for the clinical form of progressive MS
[9] and there is a particular need for new strategies to treat patients with this form of MS. Management of progressive MS, therefore, merely aims to minimize the symptoms, prevent exacerbations, and if possible, improve function. Therapies aimed at preventing the accumulation of toxic substances in the blood (Aβ or autoantibodies), or in the brain, may have therapeutic uses in AD and MS patients. Reducing amyloid deposits or reducing the amount of plaque in the brain are currently being investigated for AD treatment
[10,11,12][10][11][12]. Promising results pinpoint the reduction of the concentration of toxic substances associated with AD physiopathology, such as the Aβ peptide in the brain
[13]. Therapeutic plasma exchange apheresis (PP) is an extracorporeal blood purification technique designed to remove substances with a large molecular weight. The utility of this procedure includes the removal of antibodies, alloantibodies, immune complexes, monoclonal proteins, toxins and cytokines, and it involves the replenishment of a specific plasma factor containing 5% albumin. PP has been successfully used in several immune-mediated neurological disorders, including Guillain–Barré syndrome, chronic inflammatory demyelinating polyneuropathy, and myasthenia gravis
[14,15,16,17,18][14][15][16][17][18]. Less common neurological diseases in which plasmapheresis has afforded beneficial effects are paraneoplastic polyneuropathies, neuromyelitis optica (also known as Devic’s disease), motor neuron disease, polymyositis, and multifocal motor neuropathy
[18]. PP can be a therapeutic strategy to remove or reduce the substances that are considered pathogenically responsible, e.g., Aβ peptides in AD from the blood, by changing their transportation through the blood-brain barrier, thereby limiting their accumulation in the brain. In the case of MS, eliminating pathogenic humoral factors from the blood
[14], including suspected auto-antibodies directed against the myelin sheath, is needed in some patients with steroid refractory relapses
[15], or in patients that develop neutralizing antibodies to interferon-beta (IFN-β), which are associated with reduced bioactivity and efficacy of IFN-β
[19,20][19][20]. There is extensive literature related to the use of plasma exchange in relapsing and remitting multiple sclerosis, and its use as a temporary treatment of acute relapses in steroid-unresponsive MS patients has been recently reviewed
[15,16][15][16]. In a therapeutic plasmapheresis (plasma exchange), a volume of circulating plasma is extracted to eliminate toxic compounds, and is usually substituted by a 5% albumin solution, or occasionally by fresh frozen plasma (from donors) to replace the plasma volume removed, and thereby maintain the volemia
[15,22,25][15][21][22].