Memory Loss Not Enough to Diagnose Alzheimer’s

Summary: Researchers report on the other, often overlooked, symptoms of Alzheimer’s disease.

Source: Norhtwestern.

Relying on clinical symptoms of memory loss to diagnose Alzheimer’s disease may miss other forms of dementia caused by Alzheimer’s that don’t initially affect memory, reports a new Northwestern Medicine study.

“These individuals are often overlooked in clinical trial designs and are missing out on opportunities to participate in clinical trials to treat Alzheimer’s,” said first study author Emily Rogalski, associate professor at Northwestern’s Cognitive Neurology and Alzheimer’s Disease Center.

There is more than one kind of Alzheimer’s disease. Alzheimer’s can cause language problems, disrupt an individual’s behavior, personality and judgment or even affect someone’s concept of where objects are in space.

If it affects personality, it may cause lack of inhibition. “Someone who was very shy may go up to grocery store clerk — who is a stranger — and try to give her a hug or kiss,” Rogalski said.

This all depends on what part of the brain it attacks. A definitive diagnosis can only be achieved with an autopsy. Emerging evidence suggests an amyloid PET scan, an imaging test that tracks the presence of amyloid — an abnormal protein whose accumulation in the brain is a hallmark of Alzheimer’s — may be used during life to determine the likelihood of Alzheimer’s disease pathology.

In the study, the authors identify the clinical features of individuals with primary progressive aphasia (PPA), a rare dementia that causes progressive declines in language abilities due to Alzheimer’s disease. Early on in PPA, memory and other thinking abilities are relatively intact.

Image shows an alzheimer's brain.
There is more than one kind of Alzheimer’s disease. Alzheimer’s can cause language problems, disrupt an individual’s behavior, personality and judgment or even affect someone’s concept of where objects are in space. NeuroscienceNews.com image is for illustrtive purposes only.

PPA can be caused either by Alzheimer’s disease or another neurodegenerative disease family called frontotemporal lobar degeneration. The presence of Alzheimer’s disease was assessed in this study by amyloid PET imaging or confirmed by autopsy.

The study demonstrates that knowing an individual’s clinical symptoms isn’t sufficient to determine whether someone has PPA due to Alzheimer’s disease or another type of neurodegenerative disease. Therefore, biomarkers, such as amyloid PET imaging, are necessary to identify the neuropathological cause, the authors said.

Northwestern scientists looked at individuals in mild stages of language loss caused by Alzheimer’s disease and described their brain atrophy based on MRI scans and their results on cognitive tests.

“We wanted to describe these individuals to raise awareness about the early clinical and brain features of PPA to develop metrics which would advocate for their inclusion in clinical trials targeting Alzheimer’s disease,” Rogalski said. “These individuals are often excluded because they don’t have memory deficits, but they share the same disease [Alzheimer’s] that’s causing their symptoms.”

About this Alzheimer’s disease research article

Dr. Marsel Mesulam, director of the Cognitive Neurology and Alzheimer’s Disease Center and the Ruth Dunbar Davee Professor of Neuroscience at Northwestern University Feinberg School of Medicine, is senior author of the paper.

Funding: The study was funded by grants DC008552 from the National Institute on Deafness and Other Communication Disorders, AG13854 from the National Institute on Aging, NS075075 from the National Institute of Neurological Disorders and Stroke, all of the National Institutes of Health.

Source: Marla Paul – Norhtwestern
Image Source: This NeuroscienceNews.com image is in the public domain.
Original Research: Abstract for “Aphasic variant of Alzheimer disease” by Emily Rogalski, PhD, Jaiashre Sridhar, MS, Benjamin Rader, BA, Adam Martersteck, BS, Kewei Chen, PhD, Derin Cobia, PhD, Cynthia K. Thompson, PhD, Sandra Weintraub, PhD, Eileen H. Bigio, MD and M.-Marsel Mesulam, MD in Neurology. Published online August 26 2016 doi:10.1212/WNL.0000000000003165

Cite This NeuroscienceNews.com Article

[cbtabs][cbtab title=”MLA”]Norhtwestern . “Memory Loss Not Enough to Diagnose Alzheimer’s.” NeuroscienceNews. NeuroscienceNews, 13 September 2016.
<https://neurosciencenews.com/memory-loss-alzheimers-5034/>.[/cbtab][cbtab title=”APA”]Norhtwestern . (2016, September 13). Memory Loss Not Enough to Diagnose Alzheimer’s. NeuroscienceNews. Retrieved September 13, 2016 from https://neurosciencenews.com/memory-loss-alzheimers-5034/[/cbtab][cbtab title=”Chicago”]Norhtwestern . “Memory Loss Not Enough to Diagnose Alzheimer’s.” https://neurosciencenews.com/memory-loss-alzheimers-5034/ (accessed September 13, 2016).[/cbtab][/cbtabs]


Abstract

Aphasic variant of Alzheimer disease

Objective: To identify features of primary progressive aphasia (PPA) associated with Alzheimer disease (AD) neuropathology. A related objective was to determine whether logopenic PPA is a clinical marker for AD.

Methods: A total of 139 prospectively enrolled participants with a root diagnosis of PPA constituted the reference set. Those with autopsy or biomarker evidence of AD, and who had been evaluated at mild disease stages (Aphasia Quotient ≥85), were included (n = 19). All had quantitative language testing and APOE genotyping. Fifteen had MRI morphometry.


Results:
Impaired word-finding was the universal presenting complaint in the aphasic AD group. PPA clinical subtype was logopenic (n = 13) and agrammatic (n = 6). Fluency, repetition, naming, and grammaticality ranged from preserved to severely impaired. All had relative preservation of word comprehension. Eight of the 15 aphasic participants with AD showed no appreciable cortical atrophy at the individual level on MRI. As a group, atrophy was asymmetrically concentrated in the left perisylvian cortex. APOE ε4 frequency was not elevated.

Conclusions: There is a close, but not obligatory, association between logopenic PPA and AD. No language measure, with the possible exception of word comprehension, can confirm or exclude AD in PPA. Biomarkers are therefore essential for diagnosis. Asymmetry of cortical atrophy and normal APOE ε4 prevalence constitute deviations from typical AD. These and additional neuropathologic features suggest that AD has biological subtypes, one of which causes PPA. Better appreciation of this fact should promote the inclusion of individuals with PPA and positive AD biomarkers into relevant clinical trials.

“Aphasic variant of Alzheimer disease” by Emily Rogalski, PhD, Jaiashre Sridhar, MS, Benjamin Rader, BA, Adam Martersteck, BS, Kewei Chen, PhD, Derin Cobia, PhD, Cynthia K. Thompson, PhD, Sandra Weintraub, PhD, Eileen H. Bigio, MD and M.-Marsel Mesulam, MD in Neurology. Published online August 26 2016 doi:10.1212/WNL.0000000000003165

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