Frequently asked questions

What is Alzheimer's Disease?


Alzheimer’s disease (AD) is a brain degeneration that is associated with aging. Alzheimer's disease develops slowly and often starts with short-term memory impairment. People with Alzheimer's disease experience memory loss; they may get lost or lose things and eventually have difficulties with language, recognizing family and friends and making decisions. People with Alzheimer's disease often experience changes in their behavior and personality. The symptoms are related to the death of neurons and connections in specific regions of the brain. AD is one of a group of disorders called "dementias" that are characterized by cognitive and behavioral problems. AD is by far the most common form of dementia and accounts for ~ 75% of dementia cases, either by itself or in combination with other disorders. The overall prevalence of AD in the community is estimated to be ~ 10%. Most cases of Alzheimer's disease are diagnosed after the age of 65. Key Research Publications on Alzheimer’s disease: McKee AC, Kosik KS, Kowall NW: Neuritic pathology and dementia in Alzheimer's disease. Annals of Neurology, 1991; 30: 156-65 McKee AC, Kowall NW, Kosik KS: Hippocampal neurons predisposed to neurofibrillary tangle formation are enriched in type II Ca/calmodulin-dependent protein kinase. J Neuropathol Exp Neurol, 1990; 49: 49-63. McKee, AC, Au R, Cabral HJ, Kowall NW, Seshadri, S, Kubilus C, Drake J, Wolf P. Visual Association Pathology in Preclinical AD. Journal Neuropath Exp Neurol June; 65(6): 621-630.




What is Amyotrophic Lateral Sclerosis (ALS)


Amyotrophic Lateral Sclerosis (ALS), also known as “Lou Gehrig’s Disease,” is a progressive neurodegenerative disease of the motor neurons in the brain and spinal cord. The loss of motor neurons leads to loss of muscle movement. Signs of early ALS include weakness of the arms or legs and difficulty speaking, breathing and swallowing. The muscles may eventually decrease in size or atrophy. ALS involves the loss of voluntary muscle movements. The heart and digestive muscles are not affected. The causes of ALS are not yet fully understood, but one type of ALS has been associated with CTE and may be triggered by repetitive trauma to the head or neck. Dr. McKee's team has found that approximately 6% of people diagnosed with ALS have ALS plus CTE and 6% of people diagnosed with CTE have ALS plus CTE. All people with ALS plus CTE had a history of repetitive hits to the head from contact sports, military service or civilian life. The overall incidence of all forms of ALS is two per 100,000 people, with an average life expectancy of two to five years following diagnosis. Key Research Publications on Amyotrophic Lateral Sclerosis and CTE: McKee A,Gavett B, Stern R, Nowinski C, Cantu R, Kowall N, Perl D, Hedley-Whyte E, Price B, Sullivan C, Morin P, Lee H-S, Kubilus C, Daneshvar D, Wulff M, Budson A. TDP-43 Proteinopathy and Motor Neuron Disease in Chronic Traumatic Encephalopathy, Journal Neuropathol Exp Neurol, 2010, 69: 918-929.Factor-Litvak P, Al-Chalabi A, Ascherio A, Bradley W, Chío A, Garruto R, Hardiman O, Kamel F, Kasarskis E, McKee A, Nakano I, Nelson LM, Eisen A. Current pathways for epidemiological research in amyotrophic lateral sclerosis. Amyotroph Lateral Scler Frontotemporal Degener. 2013 May;14 Suppl 1:33-43. [PDF] WaltG, BurrisH, Brady C, Spencer K, Alvarez V, Huber B, Guilderson L, Rauf A, CollinsD, Singh T, MathiasR, AverillJ, WalkerS, RobeyI, McKee Ann, Kowall N, Stein T. Chronic traumatic encephalopathy within an amyotrophic lateral sclerosis brain bank cohort. J Neuropath Exp Neurol, 2018, Dec 1;77(12):1091-1100.




What is Chronic Traumatic Encephalopathy?


Chronic Traumatic Encephalopathy (CTE) is a progressive degenerative disease of the brain found in people with a history of repetitive brain trauma, including symptomatic concussions as well as asymptomatic subconcussive hits to the head. CTE has been found in athletes, military veterans, victims of domestic violence and others who experienced multiple falls or injuries. CTE has been known to affect boxers since the 1920’s (it was initially termed punch drunk syndrome or dementia pugilistica), but more recently has been found in players of American football, ice hockey, rugby, soccer, MMA, professional wrestling and other contact sports.CTE is not limited to professional athletes; it has also been found in athletes who did not play sports after high school or college. The repeated brain trauma triggers progressive degeneration of the brain, including loss of cells and their connections and the build-up of an abnormal protein called tau. These changes in the brain can begin months, years, or decades after the last brain trauma or end of active athletic participation. Common symptoms of CTE include memory loss, confusion, impaired judgment, impulsivity, aggression, depression, suicidality, parkinsonism, and dementia. In the photographs below, the brain tissue has been immunostained for tau protein, which appears as a dark brown color. The images on the left are from a normal person (or control), the images in the middle are from John Grimsley, a 9 year veteran of the NFL who was the first NFL player diagnosed by Dr. McKee with CTE, and the images on the right are from Paul Pender, a world champion boxer who was Dr. McKee's first case of CTE, diagnosed in 2003. The clinicopathological findings found in Paul Pender, John Grimsley and a third boxer formed the basis of Dr. McKee's first paper on CTE published in the Journal of Neuropathology and Experimental Neurology in 2009. The paper is the most highly cited paper ever published by the journal. Key Publications on CTE

McKee AC, Cantu RC, Nowinski CJ, Hedley-Whyte ET, Gavett BE, Budson AE, Santini VE, Lee H-Y, Kubilus CA, Stern RA. Chronic Traumatic Encephalopathy in Athletes: Progressive Tauopathy following Repetitive Head Injury. J Neuropath Exp Neurol, 2009 68(7): 709-735.

McKee AC, Stein TD, Nowinski CJ, Stern RA, Daneshvar DH, Alvarez VE, Lee H-S, Hall GF, Wojtowicz SM, Baugh CM, David O. Riley DO, Kubilus CA, Cormier KA, Jacobs MA, Martin BR, Abraham CR, Ikezu T, Reichard RR, Wolozin BL, Budson AE, Goldstein LE, Kowall NW, Cantu RC. The Spectrum of Disease in Chronic Traumatic Encephalopathy, Brain 2013, Jan;136(Pt 1):43-64. doi: 10.1093/brain/aws307.

McKeeAC,CairnsNJ, DicksonDW, FolkerthRD,KeeneCD, Litvan I,PerlDP, Stein TD, StewartW,VonsattelJP,TripodisY, Alvarez VE,Bieniek KF, CraryJ,Dams-O'Connor K, GordonW and the TBI/CTE group. The First NINDS/NIBIB Consensus Meeting to Define Neuropathological Criteria for the Diagnosis of Chronic Traumatic Encephalopathy. Acta Neuropathol. 2016 Jan;131(1):75-86. doi: 10.1007/s00401-015-1515-z.

Mez J, Daneshvar D, Kiernan P, Abdolmohammadi B, Alvarez V, Huber B, Alosco M, Solomon T, Nowinski C, McHale L, Cormier K, Kubilus C, Martin B, Murphy L, Baugh C, Montenigro P, Chaisson C, Tripodis Y, Kowall N, Weuve J, McClean M, Cantu R, Goldstein L, Katz D, Stern R, Stein T, McKee AC. Clinicopathological Evaluation of Chronic Traumatic Encephalopathy in Players of American Football. JAMA. 2017 Jul 25;318(4):360-370. doi: 10.1001/jama.2017.8334. PMID:28742910





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