The brain that forgets itself: Understanding anosognosia in Alzheimer’s

Alzheimer’s is often described as a “disease of memory.” While this description captures its most visible symptom, it oversimplifies the profound disruption it causes. The disease doesn’t just impair the ability to remember it alters the very architecture of identity. With every forgotten moment, every lost temporal landmark, the fragile fabric of the self begins to unravel. What’s at stake is not merely memory, but the continuity that allows us to recognize ourselves over time.

Early in its course, Alzheimer’s targets the hippocampus and medial temporal lobes areas essential for forming new memories. This is why recent events a visit, a conversation, a scheduled appointment are often the first to vanish. In contrast, older memories, especially from childhood or adolescence, may remain remarkably intact for years. These long-term memories rely on more widely distributed and consolidated neural networks within the neocortex. This dissociation explains why someone may forget what they had for breakfast but vividly recall a childhood scene. Alzheimer’s initially compromises recent episodic memory, making it difficult to form a “new past,” before progressively affecting other dimensions of memory and identity.

The mind’s mirror, cracked

While memory loss is the most visible sign of Alzheimer’s, one of its most puzzling symptoms is anosognosia the inability to recognize one’s own deficits. A person may forget a conversation from minutes earlier and confidently claim they have no memory problems. This disconnect between experience and awareness is not simply denial; it reflects a disruption in the brain systems that support self-awareness.

This awareness is not a monolithic function it unfolds in layers: basic monitoring of actions, reflective insight into thoughts and behaviors, and a higher-order capacity to place oneself in time, linking present experiences with past identity and future projections. This complex structure relies on one key process: detecting errors, assessing their significance, and integrating them into a coherent self-image. In Alzheimer’s, it is precisely this integrative and temporal function that begins to break down.

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In a healthy brain, the anterior regions especially the medial and orbitofrontal prefrontal cortex evaluate the personal relevance of incoming information. Meanwhile, posterior regions like the precuneus and posterior cingulate cortex compare current performance to the stored sense of self. Together, these structures form a “comparator system.” When a discrepancy is detected such as noticing increased forgetfulness they initiate an update of one’s self-image.

In Alzheimer’s, this loop is disrupted. The brain may still register the occurrence of an error, but the information no longer reaches the metacognitive circuits required to process and incorporate it. The person continues to perceive themselves as they were before the disease as if frozen in an outdated version of their self.

Neuroimaging studies confirm this model. Rosen’s team has linked atrophy in the orbitofrontal and medial prefrontal cortex to decreased awareness of deficits. Vannini and colleagues found that hypometabolism in the precuneus and posterior cingulate detectable even in the prodromal phase correlates with a lack of insight. Electrophysiological research adds that diminished “error awareness” can be objectively measured through evoked potentials along the brain’s midline long before dementia becomes clinically apparent. These findings, consolidated by Salmon and his team in a recent review, highlight that anosognosia is not just a side effect of memory loss but a distinct network syndrome.

Anosognosia is thus a symptom in its own right. It does not stem from denial, but from a brain that can no longer observe itself in action. The brain forgets that it forgets and it’s this double erasure that makes Alzheimer’s so unsettling for both patients and their loved ones.

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Anosognosia as a diagnostic compass

One of the most important discoveries in recent years is that anosognosia can be detected in the earliest stages of Alzheimer’s. Lack of awareness is not merely a byproduct of advanced memory loss it’s an early warning sign of the disease itself.

A study conducted at the Pitié-Salpêtrière Hospital by Guieysse and colleagues demonstrated this clearly. Using a questionnaire that compares patients’ self-assessments to evaluations from close relatives, the researchers found a striking discrepancy: even in the earliest stages, patients describe themselves as functioning normally, while their families report repeated memory lapses. This mismatch becomes an objective marker of anosognosia.

The study also revealed that incorporating the relatives’ observations into clinical assessments significantly improves diagnostic accuracy, allowing clinicians to distinguish between early-stage Alzheimer’s and non-pathological cognitive aging with greater precision.

Identifying this lack of insight has major clinical implications. It allows for earlier diagnosis even in individuals who might not seek help because they are unaware of their condition. It also transforms the caregiver relationship. Understanding that the person isn’t intentionally denying their symptoms but is neurologically unable to perceive them helps reduce tension, improves cooperation, and supports better care planning. In this sense, assessing anosognosia is no longer limited to academic research it becomes a practical tool for anticipating risk, tailoring care, and supporting both patients and caregivers.

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Alzheimer’s, then, is not simply a disease of memory it is a disruption of self-continuity. It doesn’t just erase the content of experience, but also the awareness that something has been lost. This double erasure of the self presents a unique challenge. The task for scientists and clinicians is now to examine what breaks and what endures so we can protect, even within decline, the deep and persistent sense of existing that never vanishes completely.

References

Guieysse, D., Dautricourt, S., Thomas-Antérion, C., Epelbaum, S., Benisty, S., Dubois, B., … & Habert, M. O. (2023). Detecting anosognosia for memory impairment in the prodromal stage of Alzheimer’s disease: The value of the HABC-M and caregiver burden. Journal of Alzheimer’s Disease, 92(2), 701-713.

Hester, R., Nestor, L., & Garavan, H. (2009). Impaired error awareness and anterior cingulate cortex hypoactivity in chronic cannabis users. Neuropsychopharmacology, 34(11), 2450-2458.

Meunier-Duperray, L., Souchay, C., Angel, L., Salmon, E., & Bastin, C. (2025). Exploring the domain specificity and the neural correlates of memory unawareness in Alzheimer’s disease. Neurobiology of aging, 148, 61–70.

Rosen, H. J., Alcantar, O., Rothlind, J., Sturm, V., Kramer, J. H., Weiner, M., & Miller, B. L. (2010). Neuroanatomical correlates of cognitive self-appraisal in neurodegenerative disease. NeuroImage, 49(4), 3358-3364.

Salmon, E., Meyer, F., Genon, S., Collette, F., & Bastin, C. (2024). Neural correlates of impaired cognitive processes underlying self-unawareness in Alzheimer’s disease. Cortex; a journal devoted to the study of the nervous system and behavior, 171, 1–12.

Vannini, P., Hanseeuw, B., Munro, C. E., Amariglio, R. E., Marshall, G. A., Rentz, D. M., … & Sperling, R. A. (2017). Anosognosia for memory deficits in mild cognitive impairment: Insight into the neural mechanism using functional MRI. Journal of Alzheimer’s Disease, 55(2), 615-622.