Biochemical Markers for Alzheimer’s and Parkinson’s Disease

Review Article

Austin J Clin Neurol 2015;2(7): 1059.

Biochemical Markers for Alzheimer’s and Parkinson’s Disease

Farías GA1,2,3*, Arata L1,2, Guzmán-Martínez L1,2, Morales I1,2, Tapia JP2,4 and Maccioni RB1,2

¹International Center for Biomedicine (ICC), Chile

²Laboratory of Cellular and Molecular Neurosciences, Chile

³Department of Neurology, University of Chile, Chile

4Faculty of Sciences, University of Chile, Chile

*Corresponding author: Farías GA, Department of Neurology, University of Chile, Santos Dumont 999, Independencia, Santiago, Chile

Received: May 04, 2015; Accepted: June 22, 2015; Published: June 28, 2015


Many biomarkers are currently being searched in neurodegenerative diseases like Alzheimer’s disease and Parkinson’s disease. These diseases share some common pathophysiological mechanisms and the presence of protein aggregates. Measurements of those proteins -like tau, amyloid-beta peptide and α-synuclein-, as well other mediators of neurodegeneration in cerebrospinal fluid and peripheral fluids have been explored as biomarkers. Here we summarize some of the available data on biochemical markers for neurodegenerative diseases, considering advantages and drawbacks of each marker and method of analysis.

Keywords: Biomarkers, Alzheimer`s Disease, Parkinson`s Disease, Protein misfolding diseases


AD: Alzheimer’s Disease; PD: Parkinson’s Disease; FTD: Frontotemporal Dementia; CBD: Corticobasal Degeneration; PSP: Progressive Supranuclear Palsy; MSA: Multiple System Atrophy; LBD: Lewy Body Dementia; PMDs: Protein Misfolding Diseases; α-syn: α-synuclein; CSF: Cerebrospinal Fluid; Aβ: Amyloid-beta Peptide; p-tau: Phosphorylated tau; AβPP: Aβ Precursor Protein; BBB: Blood-brain Barrier; miRNA: Micro RNA; mRNA: Messenger RNA; SPT: Serine Palmitoyltransferase; Sp 1: Specificity Protein 1; NINDCs: Non-inflammatory Neurological Disease Controls; EGF: Epidermal Growth Factor; CNS: Central Nervous System; TNF-α: Tumor Necrosis Factor-α; IL-1β: Interleukin-1β; IL-6: Interleukin-6; INF-γ: Interferon-γ; PGE2: Prostaglandin E2; TGFβ: Transforming Growth Factor β; IL-8: Interleukine 8


As world population grows older, age related neurodegenerative diseases like Alzheimer’s disease (AD) and Parkinson’s disease (PD) have become important public health concerns. Many other agerelated conditions also share some combination of their most striking clinical features (i.e. dementia and Parkinsonism), so differentiation between some diagnoses may be very difficult in individual patients.

Among differential diagnoses for AD and PD we can mention many forms of frontotemporal dementia (FTD), corticobasal degeneration (CBD) progressive supranuclear palsy (PSP), multiple system atrophy (MSA) and Lewy body dementia (LBD). All of the above also share the presence of protein aggregates on neuropathology, so they have been termed as protein misfolding diseases (PMDs) [1] and since tau or α-synuclein (α-syn) can be found frequently in protein aggregates, many of these diseases have been grouped as tauopathies i.e. AD, many forms of FTD, CBD and PSP [2-4] or as synucleinopathies i.e. PD, LBD and MSA [5]. Anyhow, is clear that multiple interactions exist between proteins in PMDs, so many proteins are affected in each PMD and conversely, most of the proteins described as responsible for PMDs show some degree of modification in each isolated PMD [5].

Many pathological processes appear to be related upstream in the process of protein aggregates generation, including misbalances in inflammatory responses, cell signaling and redox state. Even with all of our advances in the study of neurodegenerative processes and models of disease we have been unable to generate consensus on the true role of protein aggregates, so we still are not sure what is the true importance of protein deposition for PMDs and we don’t know if there is a common pathway or generator of the pathological process (like neuroinflammation) in some or all of these diseases, and if there is a common pathway of neurodegenerative process, we don’t fully understand what is the defining feature that initiates the deposition of one protein over the other and the neurodegenerative process of some neuronal populations over the next [6-9].

Since one of the main problems in the diagnosis of chronic neurodegenerative diseases is their late onset of symptoms many years after the disease has begun there is a big gap between initiation of pathologic processes and development of clinical symptoms. This is due to the brain extensive ability to compensate functions. This adaptive characteristic generates the problem that in most cases diagnosis is only possible late, when there is an advanced neurodegenerative process, so any present or future treatment will lose its effectiveness. Thereby, the development of suitable test able to identify diseases early, when symptoms are not so obvious has become an essential task for neurodegenerative diseases studies [10].

Citation: Farías GA, Arata L, Guzmán-Martínez L, Morales I, Tapia JP and Maccioni RB. Biochemical Markers for Alzheimer’s and Parkinson’s Disease. Austin J Clin Neurol 2015;2(7): 1059. ISSN : 2381-9154