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Neurofibrillary tangles

MedGen UID:
39273
Concept ID:
C0085400
Cell or Molecular Dysfunction; Finding
Synonyms: Neurofibrillary Tangle; Neurofibrillary Tangles; Tangle, Neurofibrillary; Tangles, Neurofibrillary
SNOMED CT: Neurofibrillary degeneration (85775002); Neurofibrillary tangle (85775002); Argentophilic neuronal inclusion (85775002); Alzheimer's neurofibrillary degeneration (85775002); Alzheimer's neurofibrillary change (85775002)
 
HPO: HP:0002185

Definition

Pathological protein aggregates formed by hyperphosphorylation of a microtubule-associated protein known as tau, causing it to aggregate in an insoluble form. [from HPO]

Term Hierarchy

Conditions with this feature

Gerstmann-Straussler-Scheinker syndrome
MedGen UID:
4886
Concept ID:
C0017495
Disease or Syndrome
Genetic prion disease generally manifests with cognitive difficulties, ataxia, and myoclonus (abrupt jerking movements of muscle groups and/or entire limbs). The order of appearance and/or predominance of these features and other associated neurologic and psychiatric findings vary. The three major phenotypes of genetic prion disease are genetic Creutzfeldt-Jakob disease (gCJD), fatal familial insomnia (FFI), and Gerstmann-Sträussler-Scheinker (GSS) syndrome. Although these phenotypes display overlapping clinical and pathologic features, recognition of these phenotypes can be useful when providing affected individuals and their families with information about the expected clinical course. The age at onset typically ranges from 50 to 60 years. The disease course ranges from a few months in gCJD and FFI to a few (up to 4, and in rare cases up to 10) years in GSS syndrome.
Supranuclear palsy, progressive, 2
MedGen UID:
324446
Concept ID:
C1836148
Disease or Syndrome
Alzheimer disease 3
MedGen UID:
334304
Concept ID:
C1843013
Disease or Syndrome
Alzheimer's disease can be classified as early-onset or late-onset. The signs and symptoms of the early-onset form appear between a person's thirties and mid-sixties, while the late-onset form appears during or after a person's mid-sixties. The early-onset form of Alzheimer's disease is much less common than the late-onset form, accounting for less than 10 percent of all cases of Alzheimer's disease.\n\nIndividuals with Alzheimer's disease usually survive 8 to 10 years after the appearance of symptoms, but the course of the disease can range from 1 to 25 years. Survival is usually shorter in individuals diagnosed after age 80 than in those diagnosed at a younger age. In Alzheimer's disease, death usually results from pneumonia, malnutrition, or general body wasting (inanition).\n\nAs the disorder progresses, some people with Alzheimer's disease experience personality and behavioral changes and have trouble interacting in a socially appropriate manner. Other common symptoms include agitation, restlessness, withdrawal, and loss of language skills. People with Alzheimer's disease usually require total care during the advanced stages of the disease.\n\nMemory loss is the most common sign of Alzheimer's disease. Forgetfulness may be subtle at first, but the loss of memory worsens over time until it interferes with most aspects of daily living. Even in familiar settings, a person with Alzheimer's disease may get lost or become confused. Routine tasks such as preparing meals, doing laundry, and performing other household chores can be challenging. Additionally, it may become difficult to recognize people and name objects. Affected people increasingly require help with dressing, eating, and personal care.\n\nAlzheimer's disease is a degenerative disease of the brain that causes dementia, which is a gradual loss of memory, judgment, and ability to function. This disorder usually appears in people older than age 65, but less common forms of the disease appear earlier in adulthood.
Niemann-Pick disease, type C2
MedGen UID:
335942
Concept ID:
C1843366
Disease or Syndrome
Niemann-Pick disease type C (NPC) is a slowly progressive lysosomal disorder whose principal manifestations are age dependent. The manifestations in the perinatal period and infancy are predominantly visceral, with hepatosplenomegaly, jaundice, and (in some instances) pulmonary infiltrates. From late infancy onward, the presentation is dominated by neurologic manifestations. The youngest children may present with hypotonia and developmental delay, with the subsequent emergence of ataxia, dysarthria, dysphagia, and, in some individuals, epileptic seizures, dystonia, and gelastic cataplexy. Although cognitive impairment may be subtle at first, it eventually becomes apparent that affected individuals have a progressive dementia. Older teenagers and young adults may present predominantly with apparent early-onset dementia or psychiatric manifestations; however, careful examination usually identifies typical neurologic signs.
GRN-related frontotemporal lobar degeneration with Tdp43 inclusions
MedGen UID:
375285
Concept ID:
C1843792
Disease or Syndrome
The spectrum of GRN frontotemporal dementia (GRN-FTD) includes the behavioral variant (bvFTD), primary progressive aphasia (PPA; further subcategorized as progressive nonfluent aphasia [PNFA] and semantic dementia [SD]), and movement disorders with extrapyramidal features such as parkinsonism and corticobasal syndrome (CBS). A broad range of clinical features both within and between families is observed. The age of onset ranges from 35 to 87 years. Behavioral disturbances are the most common early feature, followed by progressive aphasia. Impairment in executive function manifests as loss of judgment and insight. In early stages, PPA often manifests as deficits in naming, word finding, or word comprehension. In late stages, affected individuals often become mute and lose their ability to communicate. Early findings of parkinsonism include rigidity, bradykinesia or akinesia (slowing or absence of movements), limb dystonia, apraxia (loss of ability to carry out learned purposeful movements), and disequilibrium. Late motor findings may include myoclonus, dysarthria, and dysphagia. Most affected individuals eventually lose the ability to walk. Disease duration is three to 12 years.
Alzheimer disease 4
MedGen UID:
376072
Concept ID:
C1847200
Disease or Syndrome
Alzheimer's disease is a degenerative disease of the brain that causes dementia, which is a gradual loss of memory, judgment, and ability to function. This disorder usually appears in people older than age 65, but less common forms of the disease appear earlier in adulthood.\n\nMemory loss is the most common sign of Alzheimer's disease. Forgetfulness may be subtle at first, but the loss of memory worsens over time until it interferes with most aspects of daily living. Even in familiar settings, a person with Alzheimer's disease may get lost or become confused. Routine tasks such as preparing meals, doing laundry, and performing other household chores can be challenging. Additionally, it may become difficult to recognize people and name objects. Affected people increasingly require help with dressing, eating, and personal care.\n\nAs the disorder progresses, some people with Alzheimer's disease experience personality and behavioral changes and have trouble interacting in a socially appropriate manner. Other common symptoms include agitation, restlessness, withdrawal, and loss of language skills. People with Alzheimer's disease usually require total care during the advanced stages of the disease.\n\nAlzheimer's disease can be classified as early-onset or late-onset. The signs and symptoms of the early-onset form appear between a person's thirties and mid-sixties, while the late-onset form appears during or after a person's mid-sixties. The early-onset form of Alzheimer's disease is much less common than the late-onset form, accounting for less than 10 percent of all cases of Alzheimer's disease.\n\nIndividuals with Alzheimer's disease usually survive 8 to 10 years after the appearance of symptoms, but the course of the disease can range from 1 to 25 years. Survival is usually shorter in individuals diagnosed after age 80 than in those diagnosed at a younger age. In Alzheimer's disease, death usually results from pneumonia, malnutrition, or general body wasting (inanition).
Spongiform encephalopathy with neuropsychiatric features
MedGen UID:
339812
Concept ID:
C1847650
Disease or Syndrome
Neurodegeneration with brain iron accumulation 2B
MedGen UID:
346658
Concept ID:
C1857747
Disease or Syndrome
PLA2G6-associated neurodegeneration (PLAN) comprises a continuum of three phenotypes with overlapping clinical and radiologic features: Infantile neuroaxonal dystrophy (INAD). Atypical neuroaxonal dystrophy (atypical NAD). PLA2G6-related dystonia-parkinsonism. INAD usually begins between ages six months and three years with psychomotor regression or delay, hypotonia, and progressive spastic tetraparesis. Many affected children never learn to walk or lose the ability shortly after attaining it. Strabismus, nystagmus, and optic atrophy are common. Disease progression is rapid, resulting in severe spasticity, progressive cognitive decline, and visual impairment. Many affected children do not survive beyond their first decade. Atypical NAD shows more phenotypic variability than INAD. In general, onset is in early childhood but can be as late as the end of the second decade. The presenting signs may be gait instability, ataxia, or speech delay and autistic features, which are sometimes the only evidence of disease for a year or more. Strabismus, nystagmus, and optic atrophy are common. Neuropsychiatric disturbances including impulsivity, poor attention span, hyperactivity, and emotional lability are also common. The course is fairly stable during early childhood and resembles static encephalopathy but is followed by neurologic deterioration between ages seven and 12 years. PLA2G6-related dystonia-parkinsonism has a variable age of onset, but most individuals present in early adulthood with gait disturbance or neuropsychiatric changes. Affected individuals consistently develop dystonia and parkinsonism (which may be accompanied by rapid cognitive decline) in their late teens to early twenties. Dystonia is most common in the hands and feet but may be more generalized. The most common features of parkinsonism in these individuals are bradykinesia, resting tremor, rigidity, and postural instability.
Alzheimer disease, familial early-onset, with coexisting amyloid and prion pathology
MedGen UID:
341884
Concept ID:
C1857933
Disease or Syndrome
ADan amyloidosis
MedGen UID:
396208
Concept ID:
C1861735
Disease or Syndrome
ITM2B-related cerebral amyloid angiopathy-2, also known as familial Danish dementia (FDD), is an autosomal dominant neurodegenerative disorder characterized by the progressive development of cataracts and other ocular disorders including ocular hemorrhages, hearing impairment, varying neurologic symptoms, and dementia, usually associated with paranoid reactions and temporal disturbance of consciousness. Most patients die in the fifth to sixth decade of life. Neuropathologic findings include severe widespread cerebral amyloid angiopathy, hippocampal plaques, and neurofibrillary tangles, similar to Alzheimer disease (see 104300) (summary by Vidal et al., 2000).
Alzheimer disease 2
MedGen UID:
400197
Concept ID:
C1863051
Disease or Syndrome
Individuals with Alzheimer's disease usually survive 8 to 10 years after the appearance of symptoms, but the course of the disease can range from 1 to 25 years. Survival is usually shorter in individuals diagnosed after age 80 than in those diagnosed at a younger age. In Alzheimer's disease, death usually results from pneumonia, malnutrition, or general body wasting (inanition).\n\nAlzheimer's disease can be classified as early-onset or late-onset. The signs and symptoms of the early-onset form appear between a person's thirties and mid-sixties, while the late-onset form appears during or after a person's mid-sixties. The early-onset form of Alzheimer's disease is much less common than the late-onset form, accounting for less than 10 percent of all cases of Alzheimer's disease.\n\nAs the disorder progresses, some people with Alzheimer's disease experience personality and behavioral changes and have trouble interacting in a socially appropriate manner. Other common symptoms include agitation, restlessness, withdrawal, and loss of language skills. People with Alzheimer's disease usually require total care during the advanced stages of the disease.\n\nMemory loss is the most common sign of Alzheimer's disease. Forgetfulness may be subtle at first, but the loss of memory worsens over time until it interferes with most aspects of daily living. Even in familiar settings, a person with Alzheimer's disease may get lost or become confused. Routine tasks such as preparing meals, doing laundry, and performing other household chores can be challenging. Additionally, it may become difficult to recognize people and name objects. Affected people increasingly require help with dressing, eating, and personal care.\n\nAlzheimer's disease is a degenerative disease of the brain that causes dementia, which is a gradual loss of memory, judgment, and ability to function. This disorder usually appears in people older than age 65, but less common forms of the disease appear earlier in adulthood.
Alzheimer disease type 1
MedGen UID:
354892
Concept ID:
C1863052
Disease or Syndrome
Alzheimer disease is the most common form of progressive dementia in the elderly. It is a neurodegenerative disorder characterized by the neuropathologic findings of intracellular neurofibrillary tangles (NFT) and extracellular amyloid plaques that accumulate in vulnerable brain regions (Sennvik et al., 2000). Terry and Davies (1980) pointed out that the 'presenile' form, with onset before age 65, is identical to the most common form of late-onset or 'senile' dementia, and suggested the term 'senile dementia of the Alzheimer type' (SDAT). Haines (1991) reviewed the genetics of AD. Selkoe (1996) reviewed the pathophysiology, chromosomal loci, and pathogenetic mechanisms of Alzheimer disease. Theuns and Van Broeckhoven (2000) reviewed the transcriptional regulation of the genes involved in Alzheimer disease. Genetic Heterogeneity of Alzheimer Disease Alzheimer disease is a genetically heterogeneous disorder. See also AD2 (104310), associated with the APOE*4 allele (107741) on chromosome 19; AD3 (607822), caused by mutation in the presenilin-1 gene (PSEN1; 104311) on 14q; and AD4 (606889), caused by mutation in the PSEN2 gene (600759) on 1q31. There is evidence for additional AD loci on other chromosomes; see AD5 (602096) on 12p11; AD6 (605526) on 10q24; AD7 (606187) on 10p13; AD8 (607116) on 20p; AD9 (608907), associated with variation in the ABCA7 gene (605414) on 19p13; AD10 (609636) on 7q36; AD11 (609790) on 9q22; AD12 (611073) on 8p12-q22; AD13 (611152) on 1q21; AD14 (611154) on 1q25; AD15 (604154) on 3q22-q24; AD16 (300756) on Xq21.3; AD17 (615080) on 6p21.2; and AD18 (615590), associated with variation in the ADAM10 gene (602192) on 15q21. Evidence also suggests that mitochondrial DNA polymorphisms may be risk factors in Alzheimer disease (502500). Finally, there have been associations between AD and various polymorphisms in other genes, including alpha-2-macroglobulin (A2M; 103950.0005), low density lipoprotein-related protein-1 (LRP1; 107770), the transferrin gene (TF; 190000), the hemochromatosis gene (HFE; 613609), the NOS3 gene (163729), the vascular endothelial growth factor gene (VEGF; 192240), the ABCA2 gene (600047), and the TNF gene (191160) (see MOLECULAR GENETICS).
Niemann-Pick disease, type C1
MedGen UID:
465922
Concept ID:
C3179455
Disease or Syndrome
Niemann-Pick disease type C (NPC) is a slowly progressive lysosomal disorder whose principal manifestations are age dependent. The manifestations in the perinatal period and infancy are predominantly visceral, with hepatosplenomegaly, jaundice, and (in some instances) pulmonary infiltrates. From late infancy onward, the presentation is dominated by neurologic manifestations. The youngest children may present with hypotonia and developmental delay, with the subsequent emergence of ataxia, dysarthria, dysphagia, and, in some individuals, epileptic seizures, dystonia, and gelastic cataplexy. Although cognitive impairment may be subtle at first, it eventually becomes apparent that affected individuals have a progressive dementia. Older teenagers and young adults may present predominantly with apparent early-onset dementia or psychiatric manifestations; however, careful examination usually identifies typical neurologic signs.
Autosomal recessive early-onset Parkinson disease 23
MedGen UID:
896607
Concept ID:
C4225186
Disease or Syndrome
Parkinson disease-23 is a progressive neurodegenerative disorder characterized by young-adult onset of parkinsonism associated with progressive cognitive impairment leading to dementia and dysautonomia. Some individuals have additional motor abnormalities. Affected individuals become severely disabled within a few decades (summary by Lesage et al., 2016).
Alzheimer disease 9
MedGen UID:
924255
Concept ID:
C4282179
Finding
Supranuclear palsy, progressive, 1
MedGen UID:
1640811
Concept ID:
C4551863
Disease or Syndrome
The spectrum of clinical manifestations of MAPT-related frontotemporal dementia (MAPT-FTD) has expanded from its original description of frontotemporal dementia and parkinsonian manifestations to include changes in behavior, motor function, memory, and/or language. A recent retrospective study suggested that the majority of affected individuals have either behavioral changes consistent with a diagnosis of behavioral variant FTD (bvFTD) or, less commonly, a parkinsonian syndrome (i.e., progressive supranuclear palsy, corticobasal syndrome, or Parkinson disease). Fewer than 5% of people with MAPT-FTD have primary progressive aphasia or Alzheimer disease. Clinical presentation may differ between and within families with the same MAPT variant. MAPT-FTD is a progressive disorder that commonly ends with a relatively global dementia in which some affected individuals become mute. Progression of motor impairment in affected individuals results in some becoming chairbound and others bedbound. Mean disease duration is 9.3 (SD: 6.4) years but is individually variable and can be more than 30 years in some instances.
Frontotemporal dementia and/or amyotrophic lateral sclerosis 8
MedGen UID:
1728824
Concept ID:
C5436881
Disease or Syndrome
Frontotemporal dementia and/or amyotrophic lateral sclerosis-8 (FTDALS8) is an autosomal dominant neurodegenerative disorder characterized by adult-onset dementia manifest as memory impairment, executive dysfunction, and behavioral or personality changes. Some patients may develop ALS or parkinsonism. Neuropathologic studies show frontotemporal lobar degeneration (FTLD) with tau (MAPT; 157140)- and TDP43 (605078)-immunoreactive inclusions (summary by Dobson-Stone et al., 2020). For a discussion of genetic heterogeneity of FTDALS, see FTDALS1 (105550).

Professional guidelines

PubMed

Vaz M, Silvestre S
Eur J Pharmacol 2020 Nov 15;887:173554. Epub 2020 Sep 15 doi: 10.1016/j.ejphar.2020.173554. PMID: 32941929
Long JM, Holtzman DM
Cell 2019 Oct 3;179(2):312-339. Epub 2019 Sep 26 doi: 10.1016/j.cell.2019.09.001. PMID: 31564456Free PMC Article
Weller J, Budson A
F1000Res 2018;7 Epub 2018 Jul 31 doi: 10.12688/f1000research.14506.1. PMID: 30135715Free PMC Article

Recent clinical studies

Etiology

Ferrer I
Brain Pathol 2023 Jan;33(1):e13122. Epub 2022 Oct 12 doi: 10.1111/bpa.13122. PMID: 36223647Free PMC Article
Meneses A, Koga S, O'Leary J, Dickson DW, Bu G, Zhao N
Mol Neurodegener 2021 Dec 20;16(1):84. doi: 10.1186/s13024-021-00503-x. PMID: 34930382Free PMC Article
Ashrafian H, Zadeh EH, Khan RH
Int J Biol Macromol 2021 Jan 15;167:382-394. Epub 2020 Dec 2 doi: 10.1016/j.ijbiomac.2020.11.192. PMID: 33278431
Flowers SA, Rebeck GW
Neurobiol Dis 2020 Mar;136:104724. Epub 2020 Jan 3 doi: 10.1016/j.nbd.2019.104724. PMID: 31911114Free PMC Article
Braak H, Thal DR, Ghebremedhin E, Del Tredici K
J Neuropathol Exp Neurol 2011 Nov;70(11):960-9. doi: 10.1097/NEN.0b013e318232a379. PMID: 22002422

Diagnosis

Trejo-Lopez JA, Yachnis AT, Prokop S
Neurotherapeutics 2022 Jan;19(1):173-185. Epub 2021 Nov 2 doi: 10.1007/s13311-021-01146-y. PMID: 34729690Free PMC Article
DeTure MA, Dickson DW
Mol Neurodegener 2019 Aug 2;14(1):32. doi: 10.1186/s13024-019-0333-5. PMID: 31375134Free PMC Article
Bloom GS
JAMA Neurol 2014 Apr;71(4):505-8. doi: 10.1001/jamaneurol.2013.5847. PMID: 24493463
Serrano-Pozo A, Frosch MP, Masliah E, Hyman BT
Cold Spring Harb Perspect Med 2011 Sep;1(1):a006189. doi: 10.1101/cshperspect.a006189. PMID: 22229116Free PMC Article
Armstrong RA
Folia Neuropathol 2009;47(4):289-99. PMID: 20054780

Therapy

Vaz M, Silvestre S
Eur J Pharmacol 2020 Nov 15;887:173554. Epub 2020 Sep 15 doi: 10.1016/j.ejphar.2020.173554. PMID: 32941929
Long JM, Holtzman DM
Cell 2019 Oct 3;179(2):312-339. Epub 2019 Sep 26 doi: 10.1016/j.cell.2019.09.001. PMID: 31564456Free PMC Article
Ozben T, Ozben S
Clin Biochem 2019 Oct;72:87-89. Epub 2019 Apr 4 doi: 10.1016/j.clinbiochem.2019.04.001. PMID: 30954437
Sevigny J, Chiao P, Bussière T, Weinreb PH, Williams L, Maier M, Dunstan R, Salloway S, Chen T, Ling Y, O'Gorman J, Qian F, Arastu M, Li M, Chollate S, Brennan MS, Quintero-Monzon O, Scannevin RH, Arnold HM, Engber T, Rhodes K, Ferrero J, Hang Y, Mikulskis A, Grimm J, Hock C, Nitsch RM, Sandrock A
Nature 2016 Sep 1;537(7618):50-6. doi: 10.1038/nature19323. PMID: 27582220
Bloom GS
JAMA Neurol 2014 Apr;71(4):505-8. doi: 10.1001/jamaneurol.2013.5847. PMID: 24493463

Prognosis

Trejo-Lopez JA, Yachnis AT, Prokop S
Neurotherapeutics 2022 Jan;19(1):173-185. Epub 2021 Nov 2 doi: 10.1007/s13311-021-01146-y. PMID: 34729690Free PMC Article
Knopman DS, Amieva H, Petersen RC, Chételat G, Holtzman DM, Hyman BT, Nixon RA, Jones DT
Nat Rev Dis Primers 2021 May 13;7(1):33. doi: 10.1038/s41572-021-00269-y. PMID: 33986301Free PMC Article
Dujardin S, Commins C, Lathuiliere A, Beerepoot P, Fernandes AR, Kamath TV, De Los Santos MB, Klickstein N, Corjuc DL, Corjuc BT, Dooley PM, Viode A, Oakley DH, Moore BD, Mullin K, Jean-Gilles D, Clark R, Atchison K, Moore R, Chibnik LB, Tanzi RE, Frosch MP, Serrano-Pozo A, Elwood F, Steen JA, Kennedy ME, Hyman BT
Nat Med 2020 Aug;26(8):1256-1263. Epub 2020 Jun 22 doi: 10.1038/s41591-020-0938-9. PMID: 32572268Free PMC Article
Silva MVF, Loures CMG, Alves LCV, de Souza LC, Borges KBG, Carvalho MDG
J Biomed Sci 2019 May 9;26(1):33. doi: 10.1186/s12929-019-0524-y. PMID: 31072403Free PMC Article
Piaceri I, Nacmias B, Sorbi S
Front Biosci (Elite Ed) 2013 Jan 1;5(1):167-77. doi: 10.2741/e605. PMID: 23276979

Clinical prediction guides

Gómez-Isla T, Frosch MP
Nat Rev Neurol 2022 Jun;18(6):323-332. Epub 2022 Mar 24 doi: 10.1038/s41582-022-00642-9. PMID: 35332316Free PMC Article
Karran E, De Strooper B
Nat Rev Drug Discov 2022 Apr;21(4):306-318. Epub 2022 Feb 17 doi: 10.1038/s41573-022-00391-w. PMID: 35177833
Trejo-Lopez JA, Yachnis AT, Prokop S
Neurotherapeutics 2022 Jan;19(1):173-185. Epub 2021 Nov 2 doi: 10.1007/s13311-021-01146-y. PMID: 34729690Free PMC Article
Honig LS, Vellas B, Woodward M, Boada M, Bullock R, Borrie M, Hager K, Andreasen N, Scarpini E, Liu-Seifert H, Case M, Dean RA, Hake A, Sundell K, Poole Hoffmann V, Carlson C, Khanna R, Mintun M, DeMattos R, Selzler KJ, Siemers E
N Engl J Med 2018 Jan 25;378(4):321-330. doi: 10.1056/NEJMoa1705971. PMID: 29365294
Graham WV, Bonito-Oliva A, Sakmar TP
Annu Rev Med 2017 Jan 14;68:413-430. doi: 10.1146/annurev-med-042915-103753. PMID: 28099083

Recent systematic reviews

Inyang D, Saumtally T, Nnadi CN, Devi S, So PW
Int J Mol Sci 2023 Jun 15;24(12) doi: 10.3390/ijms241210176. PMID: 37373321Free PMC Article
Abdulrahman H, van Dalen JW, den Brok M, Latimer CS, Larson EB, Richard E
Alzheimers Dement 2022 Nov;18(11):2308-2326. Epub 2022 Jun 27 doi: 10.1002/alz.12707. PMID: 35758526Free PMC Article
Naomi R, Embong H, Othman F, Ghazi HF, Maruthey N, Bahari H
Nutrients 2021 Dec 22;14(1) doi: 10.3390/nu14010020. PMID: 35010895Free PMC Article
Lilamand M, Porte B, Cognat E, Hugon J, Mouton-Liger F, Paquet C
Alzheimers Res Ther 2020 Apr 14;12(1):42. doi: 10.1186/s13195-020-00615-4. PMID: 32290868Free PMC Article
Brown EE, Iwata Y, Chung JK, Gerretsen P, Graff-Guerrero A
J Alzheimers Dis 2016 Sep 6;54(2):615-33. doi: 10.3233/JAD-160401. PMID: 27497481

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