Diagnostic Framework: From
Dementia to Neurocognitive Disorder
In the era of the DSM-5-TR,
the traditional term dementia has been replaced with the more
scientifically precise concept of Major Neurocognitive Disorder. This shift is
not merely semantic; rather, it reflects a deeper understanding of the specific
cognitive domains affected while also removing the misconception that such
conditions occur exclusively in older adults or are inevitably degenerative.
To establish a diagnosis,
clinicians must identify significant cognitive decline from a previous level of
functioning in at least one of six core cognitive domains: complex attention,
executive function, learning and memory, language, perceptual, motor function,
or social cognition. Importantly, these impairments must be severe enough to
interfere with independence in everyday activities.
In cases such as Arthur’s,
impairments in executive function often produce particularly devastating
consequences. He may not only forget the names of loved ones but also lose the
ability to plan or carry out complex, multi-step tasks. Another crucial clinical
feature is that patients frequently demonstrate a lack of insight into their
own condition. For this reason, assessing the severity of impairment cannot
rely solely on patient self-report; it must be supplemented with objective
observations from family members and standardized neuropsychological testing.
The Amyloid Hypothesis: Three
Decades of Dominance and the Tremor of Scientific Scandal
Since Alois Alzheimer first
identified dark plaques between neurons in the brains of patients in the early
1900s, medicine believed it had discovered a key clue to understanding the
disease. By the 1990s, the Amyloid Cascade Hypothesis had become the dominant
theory in neuroscience, proposing that the abnormal accumulation of
beta-amyloid protein directly triggers neuronal death and the cognitive
symptoms associated with dementia.
The dominance of this hypothesis
shaped enormous research investment. Over the past three decades, billions of
dollars have been poured into hundreds of clinical trials designed to eliminate
or inhibit amyloid accumulation. Yet clinical reality has delivered a sobering
result: nearly all amyloid-targeting interventions have failed. Even when
modern antibody therapies successfully reduce amyloid plaque levels in the
brain, patients’ cognitive functioning often shows little improvement. In some
trials, cognitive decline has even progressed more rapidly compared with
control groups.
Amid this impasse, a soluble
amyloid oligomer known as Aβ*56 was introduced in a 2006 study by Sylvain
Lesné, presented as a potential molecular smoking gun responsible for memory
impairment. This discovery briefly revived hope that the amyloid hypothesis
could still explain Alzheimer’s pathology. However, the field was shaken again
in 2022 when a detailed investigation revealed evidence of manipulated Western
blot image data in several of Lesné’s publications. The revelation cast serious
doubt on the reliability of related findings and suggested that the scientific
community may have spent decades pursuing a misleading direction, while the
true mechanisms underlying Alzheimer’s disease might lie in alternative
pathways that remain insufficiently explored.
When Love Becomes the Antidote:
Psychosocial Interventions in Alzheimer’s Care
While biologists continue to
investigate the molecular mechanisms of disease-related proteins, psychologist
Tom Kitwood proposed a different perspective through the model of
person-centered care. Kitwood argued that the deterioration experienced by
individuals with dementia is not solely the result of neurological damage; it
is often exacerbated by what he termed malignant social psychology, patterns of
interaction that isolate patients, strip them of autonomy, and treat them as
though they have lost their personhood.
Rather than focusing exclusively on
deficits, this approach emphasizes meeting five fundamental psychosocial needs
of individuals with dementia: comfort, attachment, inclusion, occupation, and
identity. These needs converge around a central principle, love, unconditional
acceptance, and deep empathy.
When these psychosocial needs are
met, individuals with Alzheimer’s disease may gradually emerge from the shadows
of fear, confusion, and anger. In doing so, they can regain moments of
emotional harmony and peace, like returning home to a mist-filled garden of
memories where their personhood is still recognized and protected until the
very end.
Conclusion
Arthur’s story reminds us that
Alzheimer’s disease is not merely a biological problem of proteins and plaques
within the brain. It is also a profound human experience in which cognitive
decline intertwines with an enduring effort to preserve identity and dignity.
The ongoing debates surrounding the amyloid hypothesis illustrate that science
is still searching for a comprehensive explanation of the disease’s underlying
mechanisms. Yet even while biological answers remain incomplete, psychology
offers a crucial insight: the way we treat individuals living with Alzheimer’s
can profoundly shape the quality of their remaining life.
Person-centered care emphasizes
that behind behaviors that may appear confusing or difficult lies a human being
with fundamental psychological needs for connection, safety, and recognition.
When families, caregivers, and communities approach Alzheimer’s disease with
empathy rather than solely with diagnostic labels, they do more than reduce
suffering, they help safeguard the remaining fragments of the individual’s
personhood.
References
American Psychiatric Association.
(2022). Diagnostic and statistical manual of mental disorders (5th ed.,
text rev.). https://doi.org/10.1176/appi.books.9780890425787
Barron, S. (2025).
Psychopharmacology. In R. Biswas-Diener & E. Diener (Eds.), Noba
textbook series: Psychology. Champaign, IL: DEF Publishers.
Kitwood, T. (1997). The experience
of dementia. Aging & Mental Health, 1(1), 13–22.
Queen, T., & Smith, J. (2025).
Aging. In R. Biswas-Diener & E. Diener (Eds.), Noba textbook series:
Psychology. Champaign, IL: DEF Publishers.
Science.org. (2022). Faked
Beta-Amyloid Data. What Does It Mean?
Vasquez, K. (2025). Neurocognitive
disorders. Alverno College PSY 250.

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